The cerebellum is a central equilibrium organ and coordination of movements. It is formed by two hemispheres with a large number of grooves and sowls, and a narrow middle part - a worm.
The main mass of the gray substance in the cerebellum is located on the surface and forms it a bark. A smaller part of the gray substance lies deep in the white substance in the form of the central cerebel kernel.
In the cerebeller core distinguish 3 layers: 1) the outer molecular layer contains relatively few cells, but a lot of fibers. It distinguishes basket and star neurons that are brakes. Star - brake vertical, baskets - send axons over long distances that end on the bodies of pear cells. 2) The average ganglionary layer is formed by one nearby large pear cells, first described by the Czech scientist Yan Purkinier. Cells have a large body, 2-3 short dendrites are departed from the vertex, which are branched in a small layer. 1 axon, which goes into the white substance to the cerebellum kernels. 3) the inner grain layer is characterized by a large number of tightly lying cells. Among the neurons there are grain cells, Golgi cells (star), and spindle horizontal neurons. Cell-grain - small cells that have short dendrites, the latter are formed with mossoid fibers exciting synapses in glamoruras of the cerebellum. The grain cells excite the mossoid fibers, and the axons go into the molecular layer and transmit information to pear cells and all the fibers located there. This is the only cerebellum bark neuron. Golges' cells lie under the bodies of pear-like neurons, the axons go into the glarelands of the cerebellum, can slow down the pulses with mossoid fibers on the grain cells.
In the ceremony of the cerebellum, the afferent paths of 2 types of fibers are received: 1) Lyanovoid (Lazing) - they rise from white substance C / s grainy and ganglionary layers. They reach the molecular layer, form synapses with dendrites of pear cells and they are excited. 2) Mossoid - from white substance come in a grain layer. Here form synapses with dendrites of granular cells, and axons of grainy cells go into the molecular layer, forming synapses with dendrites of pear-like neurons, which form brake kernels.
Bark big brain. Development, neuralized composition and layered organization. The concept of cyto- and myelocitectonics. Hemato-encephalic barrier. Structural and functional unit of bark.
The bark of a large brain semirapers is the highest and most complex organized nervous center of the screen type, whose activity provides the regulation of various functions of the body and complex forms of behavior. The bark is formed by a gray substance layer. The gray substance contains nervous cells, nerve fibers and neuroglia cells.
Among the multipolar neurons of the cortex, the pyramid, star, spindle-shaped, spider, horizontal, candelabra cells, cells with a double bouquet of dendrites and some other types of neurons are distilled.
The pyramidal neurons constitute the main and most specific cortex shape. They have an elongated cone-shaped body, the top of which is facing the surface of the bark. From the top and side surfaces of the body departure. From the base of the pyramid cells take the beginning of the axon.
The pyramidal cells of various layers of the cortex differ in size and have a different functional value. Small cells are inserting neurons. A axons of large pyramids take part in the formation of motor pyramidal pathways.
Corn neurons are located nonresopable layers, which are denoted by Roman numbers and numbered outside. Each layer is characterized by a predominance of any single cell type. In the cortex hemispics distinguish six main layers:
I - the molecular layer of the cortex contains a small amount of small associative horizontal cells of the cauchal. Their axons pass parallel to the brain surfaces in the composition of the tangential plexus of the nerve fibers of the molecular layer. However, the bulk of the fibers of this plexus is represented by branchings of dendrites of the underlying layers.
II - the outer grainy layer is formed by numerous small pyramid and star neurons. The dendrites of these cells rise into the molecular layer, and axons either go into white substance, or, forming arcs, also enter the tangential weaving of the molecular layer fibers.
III - the widest layer of big brain cortex - pyramid. It contains pyramidal neurons, and spindle-shaped cells. Apical dendrites The pyramids go into the molecular layer, the side dendrites form synapses with adjacent cells of this layer. Akson pyramid cell always departs from its base. In small cells, it remains within the bark, in large - forms a myelin fiber, which goes into the brain white substance. Axons of small polygonal cells are sent to the molecular layer. The pyramid layer performs predominantly associative functions.
IV - the inner grainy layer in some fields of the cortex is very strong (for example, in visual and auditory zones of the crust), and in others it can almost absent (for example, in a presenter urge). This layer is formed by small star neurons. It includes a large number of horizontal fibers.
V is a ganglionary layer of the crust formed by large pyramids, and the area of \u200b\u200bthe motor cortex (a presenter exposure) contains giant pyramids, which first described the Kiev Anata V. A. Betin. Apical dendrites Pyramids reach the i-th layer. AXSONS Pyramids are projected on the motor cores of the head and spinal cord. The longest axons of Betz cells in the composition of the pyramid paths reach the caudal segments of the spinal cord.
VI - a layer of polymorphic cells is formed by a variety of neurons (spindle-shaped, star). The axons of these cells go into a white substance in the composition of the efferent paths, and the dendrites reach the molecular layer.
CitoarchiteCextonic - features of the location of neurons in various parts of the large brain cortex.
Among the nerve fibers of the cortex of the Big Brain, associative fibers can be distinguished by associative fibers, connecting individual sections of the cortex of one hemisphere, the Commission connecting the bore of various hemispheres, and projection fibers, both afferent and efferent, which bind the bore with the nuclei of the lower departments of the central nervous system.
Vegetative nervous system. General structural characteristics and basic functions. The structure of sympathetic and parasympathetic reflex arcs. Differences of vegetative reflex arcs from somatic.
Represents bleachedLocated in the spinal channel, about 45 cm long in men and 42 cm in women. In the locations of the nerves to the upper and lower limbs of the spinal cord has two thickening: cervical and lumbar.
The spinal cord consists of two types of fabric: Outdoor white (beams of nerve fibers) and inner gray substance (body of nerve cells, dendrites and synapses). In the center of the gray substance along the entire brain there is a narrow canal with cerebrospinal fluid. The spinal cord has segmental structure (31-33 segments), each of its plot is associated with a certain part of the body, 31 pair of spinal from the spinal cord segments are departed. nerves: 8 cervical pairs (CI-CVIII), 12 bedroom pairs (THI-THXII), 5 pairs of lumbar (Li-LV), 5 pairs of sacral (Si-SV) and pair of cleaners (COI-COIII).
Each nerve when leaving the brain is divided into front and rear roots. Rear roots - afferent paths, front roots Efferent paths. At the rear surfaces of the spinal nerves in the spinal cord, afferent impulses come from the skin, motor apparatus, internal organs. The front roots are formed by motor nerve fibers and transmit efferent pulses to the working bodies. Sensitive nerves prevail over motor, therefore, there is a primary analysis of incoming afferent signals and the formation of the reactions of the most important for the body at the moment (the transfer of numerous afferent pulses to a limited number of efferent neurons is called convergence).
Total amount neurons of spinal cord It is about 13 million. They are subdivided: 1) in the department of the nervous system - neurons of somatic and vegetative NA; 2) for the purpose - efferent, afferent, inserts; 3) by influence - exciting and brakes.
The functions of the neurons of the spinal cord.
Efferent neuronscome on the somatic nervous system and innervate skeletal muscles - motioneons. Alpha and gamma are distinguished - motorway. A-MotoMeons Carry out the skeletal muscle of the spinal cord signals. Aksona of each motioneerone is repeated many times, so each of them covers many muscle fibers, forming a motor motor unit with it. M-MOTNEYRONES Innervat muscle muscle spindle fibers. They have a high frequency of impulsation, receive information about the effluent of muscle spindle through intermediate neurons (inserted). Generate pulses with a frequency up to 1000 per second. These are phosoactive neurons that have up to 500 synapses on their dendrites.
Afferent neurons Somatic NSs are localized in spinal ganglia and ganglia of the cranial brain nerves. Their processes are carried out impulsed from muscle, tendon, skin receptors, enter the appropriate spinal cord segments and are connected by synapses with inserted or alpha-motnelones.
Function inserts neurons It consists in organizing communication between the structures of the spinal cord.
Neurons of vegetative nervous systemare inserted . Sympathetic neurons Located in the side horns of the thoracic spinal cord, they have a rare pulsation frequency. Some of them are involved in maintaining a vascular tone, others in the regulation of the smooth muscles of the digestive system.
The totality of neurons forms nervous centers.
In the spinal cord there are regulation centers most internal organs and skeletal muscles.Centers control of skeletal muscles They are located in all spinal cord departments and innervat the skeletal muscles of the neck (CI-CIIV), the diaphragm (CIII-CV), the upper limbs (CV-THII), the torso (THIII-LI), the lower limbs (Lii-SV). In case of damage to certain segments of the spinal cord or its conductive paths, specific motor disorders and sensitivity disorders are developing.
Spinal cord functions:
A) provides a bilateral connection between the spinal nerves and the brain - the conductor function;
B) carries out complex motor and vegetative reflexes - reflex function.
It is a system of tissues and organs built from nervous tissue. It is distinguished:
Central Department: Head and Spinal Brain
Peripheral department: autonomous and sensitive ganglia, peripheral nerves, nervous endings.
There is also a division to:
Somatic (animal, cerebrospinal) department;
Vegetative (autonomous) department: sympathetic and parasympathetic parts.
The nervous system form the following embryonic sources: a nervous tube, a nerve comb (ganglion plate) and embryonic placodes. Fissure elements of shells are mesenchymal derivatives. At the stage of closure of neuropores, the front end of the tube is significantly expanding, the side walls are thickened, forming the root of three brain bubbles. The underlying cranial bubble forms the front brain, the middle bubble is the middle brain, and from the third bubble, which goes into the spinal cord laying, the rear (rhombid) brain develops. Shortly thereafter, the nerve tube bends almost at a right angle, and by means of furrow-escalation, the first bubble is divided into final and intermediate departments, and the third brain bubble - on the oblong and rear brain departments. Derivatives of the middle and rear brain bubbles form the brain barrel and are ancient formations; They maintain the segmental principle of the structure, which disappears in the derivatives of the intermediate and final brain. Integrative functions are concentrated in the latter. This is how five brain departments are formed: the final and intermediate brain, medium, oblong and rear brain (a person occurs at about the end of the 4th na of embryonic development). The final brain forms two hemispheres of a large brain.
In the embryonic histo and organogenesis of the nervous system, the development of different brain departments occurs at different speeds (heterochronically). Previously, caudal departments of the central nervous system (spinal cord, brain stem) are formed; The time of the final formation of the structures of the brain varies greatly. In a number of brain departments, this occurs after birth (cerebellum, hippocampus, olfactory bulb); In each brain department, there are spatial-temporal gradients for the formation of neural populations, which form the unique structure of the nervous center.
The spinal cord is a part of the central nervous system, in the structure of which the features of the embryonic stages of the development of vertebrate brain are most clearly preserved: the tubular nature of the structure and segmen-tar. In the side sections of the nervous tube rapidly increases the mass of cells, while the dorsal and ventral parts do not increase in volume and retain the ependium. The thickened side walls of the nervous tube are divided by a longitudinal furrow on the dorsal - wing, and the ventral is the main plate. At this stage of development, three zones can be distinguished in the lateral walls of the nervous tube: ependim, lining central channel, intermediate (cloak layer) and marginal (edge \u200b\u200bveil). A gray substance of the spinal cord is further developed from the cinema layer, and its white substance is from the regional veil. The neuroblasts of the front pillars are differentiated into the motioneons (motor neurons) of the front horns. Their axons come out of the spinal cord and form the front spinders of the spinal nerves. In the rear pilots and the intermediate zone, various kernels of insert (associative) cells are developing. Their axons, entering the white substance of the spinal cord, are part of various conductive beams. The rear horns include the central processes of sensitive neurons of the spinal nodes.
Simultaneously with the development of the spinal cord, the spinal and peripheral nodes of the autonomous nervous system are laid. The source material for them is stem cellular elements of the nervous ridge, which, by divergent differentiation, are developing in neuroblah-stick and glioblastic directions. A part of the nervous crest cells migrates to the periphery in the location of the nodes of the autonomous nervous system, paragaliyev, the neuro-endocrine cells of the APUD-series and chromaffinity tissue.
Peripheral nervous system.
The peripheral nervous system combines peripheral nerve nodes, trunks and endings.
Nervous ganglia (knots) - structures formed by the accumulations of neurons outside the CNS, are divided into sensitive and autonomous (vegetative). Sensitive ganglia contain pseudo-monolar or bipolar (in spiral and vestibular ganglia) afferent neurons and are located predominantly in the course of the rear spinal cord roots (sensitive nodes of cerebrospinal nerves) and some cranial brain nerves. Sensitive ganglia of the spinal nerves have a belief shape and covered with a capsule of dense fibrous connective tissue. According to the periphery of Ganglia, there are dense accumulations of the bodies of pseudo-monopolar neurons, and the central part is occupied by their processes and located between them with subtle layers of the endoneurry, carrier vessels. Autonomous nerve ganglias are formed by the clusters of multipolar neurons, on which numerous synapses form pregganese fibers - neuron processes, whose bodies lie in the central nervous system.
Nerve. Building and regeneration. Spinal ganglia. Morphofunctional characteristic.
Nerves (nervous trunks) bind the nerve centers of the head and spinal cord with receptors and working bodies. They are formed by the bunches of myelin and messenger fibers, which are combined with connective tissue components (shells): Endonery, perinovel and epideos. Most nerves are mixed, i.e. Includes afferent and efferent fibers.
Endionering - thin layers of loose fibrous connective tissue with fine blood vessels surrounding individual nerve fibers and bind them into a single bundle. Períneuria is a shell covering every bundle of nerve fibers outside and glowing partitions deep into the beam. It has a plate structure and images of concentric layers of flattened fibroblat-like cells associated with dense and slotted connections. Between the cell layers in the spaces filled with liquid, the components of the basal membrane and longitudinally oriented collagen fibers are located. Epidering is the outer sheath of the nerve, connecting the bunches of nerve fibers together. It consists of dense fibrous connective tissue containing fat cells, blood and lymphatic vessels.
Spinal cord. Morphofunctional characteristic. Development. The structure of gray and white substance. Neuralize.
The spinal cord consists of two symmetrical half, rewarded from each other in front of the deep middle gap, and behind the connected partition. The inner part of the organ is darker - this is his gray substance. On the periphery of the spinal cord there is a lighter white substance. The gray substance of the spinal cord consists of neuron bodies, messenger and thin myelin fibers and neuroglia. The main component of a gray substance that distinguishes it from white is multipolar neurons. The protrusions of the gray substance are called horns. Distinguish front, or ventral, rear, or dorsal, and side, or lateral, horns. In the process of developing the spinal cord from the nervous tube, neurons are formed, which are grouping in 10 layers, or in the plates. For a person characteristic
the following architectonical plates: I-V plates correspond to the backwards, the VI-VII plate - the intermediate zone, the VIII-IX plate - the front horns, x plate - the zone of the near central canal. The gray matter of the brain consists of multipolar neurons of three types. The first type of neurons is phylogenetically more ancient and characterized by a few long, straight and slightly branching dendrites (isodendritic type). The second type of neurons has a large number of highly branching dendrites, which are intertwined by forming "tangles" (idiodendritic type). The third type of neurons according to the degree of development of dendrites occupies an intermediate position between the first and second types. White spinal cord substance is a set of longitudinally oriented predominantly myelin fibers. Bunches of nervous fibers that communicate between various parts of the nervous system are called the spinal cord conduction paths
Brain. Sources of development. The total morphofunctional characteristic of large hemispheres. Neural organization of large hemispheres. Cyto and myelochetectonics of the cortex of large hemispheres of the brain. Age-related cortex.
In the brain there are gray and white substance, but the distribution of these two components here is much more complicated than in the spinal cord. Most of the gray brain gray is located on the surface of the big brain and in the cerebellum, forming their bark. A smaller part forms numerous brain cores.
Structure. The large brain bark is represented by a layer of gray matter. It is most developed in the front central winking. The abundance of furrow and the convulsive increases the area of \u200b\u200bthe gray matter of the brain. Various areas of it, different from each other by some features of the location and structure of cells (cytoarchitectonic), the location of the fibers (myelocitectonics) and the functional value are called fields. They are the highest analysis sites and the synthesis of nerve impulses. Sharply outlined
there are no boundaries between them. For the bark, the location of cells and fibers layers is characterized. The development of the bark of large hemispheses (neocortex) of a person in embryogenesis occurs from the ventricular germinative zone of the final brain, where unprofitialized proliferating cells are located. Neurochetes of neocortex are differentiated from these cells. In this case, the cells lose the ability to divide and migrate into the forming cortical record. Initially, neurocytes of future I and VI layers come to the cortex plate, i.e. The most superficial and deep layers of the crust. Then, in the direction of the V, IV, III and II, II layers, is embedded into it. This process is carried out by the formation of cells in small sections of the ventricular zone in different periods of embryogenesis (heterochron-but). In each of these areas, groups of neurons consistently arranged along one or several fibers are formed.
radial glia in the form of column.
Cytoarchitectonics of large brain bark. Multipolar cortex neurons are very diverse in shape. Among them, you can select pyramid, star, spindle-shaped, spider-shaped and horizontal neurons. Corn neurons are located nonresopable layers. Each layer is characterized by a predominance of any single cell type. In the motor zone of the cortex, 6 main layers are distinguished: I - molecular, II - outer grainy, III - Nuramidny neurons, IV - inner grainy, V - ganglionary, VI - layer of polymorphic cells. The molecular layer of the cortex contains a small amount of minor associative cells of the servers -ide form. Their neurites take place parallel to the brain surfaces in the composition of the tangential plexus of the nerve fibers of the molecular layer. The outer grainy layer is formed by small neurons having a rounded, angular and pyramidal shape, and star neurocytes. The dendrites of these cells rise into the molecular layer. Neurites or leaving in a white substance, or forming arcs, also enter the tangential plexus of the fibers of the molecular layer. The widest layer of big brain cortex is a pyramid. From the top of the pyramid cell, the main dendrite moves in the molecular layer. Neuit pyramid cell always departs from its base. Inner grainy layer is formed by small star neurons. It includes a large number of horizontal fibers. The ganglionary layer of the cortex is formed by large pyramids, and the region of a presenter winding contains gigantic pyramids.
The polymorphic cell layer is formed by neurons of various shapes.
MeloarchiteCectonic crust. Among the nerve fibers of the cortex of a large brain can be distinguished by associative fibers, connecting certain sections of the cortex of one hemisphere, the Commission connecting the bore of various hemispheres, and projection fibers, both afferent and efferent, which bind the bore with the nuclei of the lower departments of the central
nervous system.
Age-related changes. On the 1st year of life, the form of the form of pyramid and star neurons is observed, their increase, the development of dendritic and axon arborization, intransmented vertical ties. By 3 years in ensembles, "nest" neurons groupings are detected, more clearly formed vertical dendritic beams and beams of radiar fibers. By 5-6 years, polymorphism of neurons increases; The system of intracambal bonds horizontally complicates due to growth in the length and branches of lateral and basal dendrites of pyramid neurons and the development of side terminals of their apical dendrites. By 9-10 years, cell grouping increases, the structure of short-accessed neurons is significantly complicated, and the network of axonne collaterals of all forms of interneurons is expanding. By 12-14 years in ensembles, specialized forms of pyramid neurons are clearly referred to, all types of interneurons reach a high level of differentiation. By 18 years old, the ensemble organization of the bark in the main parameters of its architectonics reaches the level of such in adults.
Cerebellum. Building and morphofunctional characteristic. Neural composition of cerebellum core, glyocytes. Interneurone connections.
Cerebellum. It is a central equilibrium body and coordination of movements. It is associated with a brain barrel by afferent and efferent conductive beams forming together three pairs of brazeline legs. On the surface of the cerebellum, many convolutions and grooves, which significantly increase its area. Furrows and gyruses are created on the context
the painting of the "Tree of Life" is characteristic of the cerebellum. The main mass of the gray substance in the cerebellum is located on the surface and forms it a bark. A smaller part of the gray substance lies deep in the white substance in the form of central nuclei. In the center of each winding there is a thin layer
white substance coated with a layer of gray substance - bark. In the cerebeller core, three layers are distinguished: the outer-molecular, medium-ganglionary layer, or a layer of pear-like neurons, and internal-and-andy. The ganglion layer contains pear-like neurons. They have neurites, who, leaving the ceremony of the cerebel, form the initial link of its efferent
brake paths. 2-3 dendrites are departed from the pear-shaped body into the molecular layer, which permeate the entire thickness of the molecular layer. Neurites passing through the granular cerebellum cerebral layer in white substance and ending with cerebellum kernels are departed from the base of these cells. The molecular layer contains two main types of neurons: Corridge and star. Basket neurons are in the lower third of the molecular layer. Their thin long dendrites are branched mainly in the plane located crosswise to the urge. Long neurites of cells always go across the winding and parallel to the surface over pear-like neurons. Star neurons lie above the baskets and emey two types. Small star neurons are equipped with thin short dendrites and underdeveloped neurites forming synapses. Large star neurons have long and strong branched dendrites and neurites. Granular layer. The first type of cells of this layer can be considered grain neurons, or grain cells. The cell has 3-4 short dendrites,
end branching in the same layer in the same layer of poultry foot. Neurites of grain cells pass to the molecular layer and are divided into two branches, oriented parallel to the surface of the bark along the sowls of the cerebellum. The second type of cerebellum grain layer cells are brake large star neurons. There are two types of cells: with short and long neurites. Neurons with short neurites lie near the ganglionary layer. Their branched dendrites propagate in the molecular layer and form synapses with parallel fibers - axonse-grain cells. Neurites are sent in a grain layer to the cerebellum glomers and end with synapses on the end branches of dendrites of grain cells.
Long-term Star neurons with long neurites have abundantly branched in the granular layer of dendrites and neurites leaving in a white substance. The third type of cells make up spindle horizontal cells. They have a small elongated body, from which in both directions, long horizontal dendrites are departed, ending in the ganglionary and grain layers. Neurites of these cells give collaterals in a grain layer and go to
white substance. Glyocytes. The cerebulic cortex contains various clay elements. In the grain layer there are fibrous and protoplasmic astrocytes. The legs of the process of fibrous astrocytes form perivascular membranes. All layers in the cerebellum have oligodendrocytes. Especially rich in these cells a grain layer and a white matter of the cerebellum. In the ganglionary layer between the pear-like neurons there are clay cells with dark nuclei. The processes of these cells are directed to the surface of the cortex and form the glial fibers of the molecular layer of the cerebellum. Interneurone connections. The afferent fibers entering the ceremony of the cerebelley are represented by two species - mossoid and so-called dazing fibers. Mossoid fibers go in the composition of olive and bridges and indirectly through grain cells have an exciting effect on pear cells.
Lubing fibers enter the ceremony of the cerebellum, apparently, according to the spinal cerebellary and vestibuloscent paths. They cross the grain layer, fit to the pear-like neurons and are sprinkled by their dendrites, ending on their surface with synapses. Lubing fibers transmit excitation directly pear-like neurons.
Autonomous (vegetative) nervous system. Total morphofunctional characteristic. Departments. The structure of extramural and intramural ganglia.
VNS is divided into sympathetic and parasympathetic. Both systems simultaneously take part in the innervation of organs and have opposite effect on them. It consists of the central departments represented by the cores of the gray substance of the head and spinal cord, and peripherals: nerve trunks, nodes (ganglia) and plexuses.
Intramural ganglia and related pathways due to their high autonomy, the complexity of the organization and the features of the media exchange is allocated to an independent metacipatic department of autonomous NA. Three types of neurons are distinguished:
Longaxo efferent neurons (cell type cells I) with short dendrites and long axon, going beyond the node to the cells of the working body, on which it forms motor or secretory endings.
Equal appearance of afferent neurons (cells II cells II) contain long dendrites and axon, which is out of this ganglium into neighboring and forming synapses on cells I and III types. It is included as a receptor in the composition of local reflex arcs, which are closed without a nervous impulse at the central nervous system.
Associative cells (cells of the type of doogle) are local insertes of neurons connecting several cells of the cells in their processes. The dendrites of these cells do not go beyond the node, and axons are sent to other nodes, forming synapses on type I cells.
1.1. Nervous System: General Structure
The nervous system is a system of an organism that combines and regulating various physiological processes in accordance with the changing conditions of the external and internal environment. The nervous system consists of sensory components that react to stimuli outgoing from the environment, integrative - processing and storing sensory and other data, and motor controlling the movements and secretory activities of the glands.
The nervous system perceives sensory incentives, recycles information and forms behavior. Special types of information processing are learning and memory, due to which when environmental changes, behavior adapts to the preceding experience. These functions are also involved in other systems, such as endocrine and immune, but the nervous system is specialized to perform the specified functions. The processing of information implies the transmission of information in neural networks, transformation of signals by combining them with other signals (nervous integration), storing information in memory and extraction of information from memory, using sensory information for perception, thinking, training, planning (preparation) and motor execution teams, formation of emotions. The interactions between neurons are carried out through both electrical and chemical processes.
Behavior is a complex of organism reactions for changing conditions of the outer and internal environment. Behavior may be a purely internal, hidden process (cognition) or accessible to external observation (motor or vegetative reactions). A person is especially important a set of those behavioral acts that are associated with speech. Each reaction, simple or complex, provide nervous cells organized in neural networks (nerve ensembles and paths).
The nervous system is divided into central and peripheral (Fig. 1.1). The central nervous system (CNS) consists of a head and spinal cord. The peripheral nervous system includes roots, plexus and nerves.
Fig. 1.1.The overall structure of the nervous system.
BUT- Central nervous system. B.- Brain trunk: 1 - final brain; 2 - intermediate brain; 3 - medium brain; 4 - bridge and cerebellum, 5 - oblong brain, 6 - final brain Middle structures. AT- spinal cord: 7 - spinal cone; 8 - Terminal Threads. G.- Peripheral nervous system: 9 - ventral root; 10- Dorzal Fur; 11 - spinal ganglia; 12 - spinal nerve; 13 - mixed peripheral nerve; 14 - epineurial; 15 - perineuria; 16 - myelin nerve; 17 - Fibrocyte; 18 - Endoneurry; 19 - capillary; 20 - non-free nerve; 21 - skin receptors; 22 - ending motorway; 23 - capillary; 24 - muscle fibers; 25 - the core of the Schvanna cell; 26 - capture Ranvier; 27 - sympathetic barrel; 28 - connecting branch
central nervous system
The CNS collects and processes the information coming from receptors on the environment, formates reflexes and other behavioral reactions, plans and performs arbitrary movements. In addition, the CNS provides so-called higher cognitive (cognitive) functions. The CNS occurs processes related to memory, learning and thinking.
The brain in the process of ontogenesis is formed from brain bubbles arising from the uneven growth of the front sections of the medullary tube (Fig. 1.2). From these bubbles the front brain is formed (PROSENCEPHALON),medium brain Mesencephalon)and diamond-shaped brain (rhombencephalon).Further, the final brain forms the final (Telencephalon)and intermediate (Diencephalon)the brain, and the rhombid brain is divided into the rear (Metencephalon)and oblong Myelencephalonor mEDULLA OBLONGATA)brain. From the final brain, respectively, the heavy brain hemisphere is formed, basal ganglia, from the intermediate brain - Talamus, epitulamus, hypothalamus, metatalamus, visual paths and nerves, retina. Spectator nerves and retina - CNS departments, as if deposited beyond the brain. From the middle of the brain, the plate is formed quadruple and legs of the brain. Bridge and cerebellum are formed from the back of the brain. The brain bridge borders down to the oblong brain.
The rear of the medullary tube forms a spinal cord, and its cavity turns into the central spinal cord channel. The spinal curt consists of a cervical, thoracic, lumbar, sacrochny and spheroid departments, each of which in turn develops from segments.
The CNS distinguishes gray and white substance. The gray substance is a cluster of neurons, white substance - neuron processes covered with myelin shell. In the brain, the gray substance is in the crust of large hemispheres, in the subcorter ganglia, the cores of the brain barrel, the cerebeller core and its kernels. In the spinal cord, the gray substance is concentrated in its middle, white - on the periphery.
Peripheral nervous system
The peripheral nervous system (PNS) is responsible for the conjugation between the environment (or excitable cells) and the CNS. The PNS includes sensory (receptors and primary afferent neurons) and motor (somatic and vegetative motioneons) components.
Fig. 1.2.Embryonic development of the nervous system of a mammal. The scheme of the development of the nervous logging in the three stage (BUT)and five (B)brain bubbles. A. I.- General side view: 1 - Cranial bend; 2 - cervical bending; 3 - spinal assembly. II.- Top view: 4 - front brain; 5 - medium brain; 6 - diamond-shaped brain; 7 - neurotic; 8 - wall of the nervous tube; 9 - Required spinal cord.
B. I.- General side view. B. II.- Top view: 10 - finite brain; 11 - side ventricles; 12 - intermediate brain; 13 - eye stalk; 14 - crystal; 15 - optic nerve; 16 - medium brain; 17 - rear brain; 18 - oblong brain; 19 - spinal cord; 20 - central channel; 21 - fourth ventricle; 22 - brain water pipe; 23 - the third ventricle. III- Side view: 24 - new bark; 25 - interventricular partition; 26 - striped body; 27 - Pale ball; 28 - Hippocampus; 29 - Talamus; 30 - a sishkovoid body; 31 - upper and lower hilly; 32 - cerebellum; 33 - rear brain; 34 - spinal cord; 35 - oblong brain; 36 - bridge; 37 - medium brain; 38 - neurohypophysis; 39 - hypothalamus; 40 - almond-shaped body; 41 - olfactory tract; 42 - olfactory bark
Sensory part of PNS.Sensory perception is the transformation of an external stimulus energy into a nervous signal. It is carried out by specialized structures - receptors that perceive the effect on the body of a variety of external energy types, including mechanical, light, sound, chemical incentives, temperature changes. The receptors are located on the peripheral endings of primary afferent neurons transmitting the received information in the central nervous system on sensitive fibers of nerves, plexuses, spinal nerves and, finally, on the rear spores of the spinal cord (or by cranial nerves). The bodies of the cells of the rear roots and cranial nerves are in the spinal (spinal) ganglia or in the gangles of the cranial nerves.
Motor part of PNS.The Motor component of the PNS includes somatic and vegetative (autonomous) motioneons. Somatic motoricoons innervate the cross-and-coated muscles. The cells of the cells are in the front horns of the spinal cord or in the brain barrel, they have long dendrites that receive many synaptic "inputs". Motioneons of each muscle are a specific motor kernel - a group of CNS neurons having similar functions. For example, the muscles of the face are inherited from the nucleus of the facial nerve. A axons of somatic motioneons leave the central nervous system through the front root either through the cranial nerve.
Vegetative (autonomous) motioneonsseparate nerves to the fibers of smooth muscles and to the glands - pregganionic and postganglyonary neurons of the sympathetic and parasympathetic nervous system. Pregganionic neurons are located in the central nervous system - in the spinal curtain or in the brain barrel. In contrast to somatic motionones, vegetative pregglicion neurons form synapses not on the effector cells (smooth muscles or glands), and in postganglyonary neurons, which, in turn, synaptically contact directly with the effectors.
1.2. Microscopic structure of the nervous system
The base of the nervous system is nervous cells, or neurons specializing in obtaining incoming signals and to transmit signals to other neurons or effector cells. In addition to nerve cells, in the nervous system there are clay cells and connecting tissue elements. Neuroglia cells (from Greek. Glia - Glue)
linger in the nervous system of support, trophic, regulatory functions, participating in almost all types of neurons activity. Quantitatively, they prevail over neurons and occupy the entire volume between vessels and nerve cells.
Nerve cell
The main structural functional unit of the nervous system is neuron (Fig. 1.3). In neuron, the body is distinguished (soma) and processes: dendrites and axon. Soma and dendrites represent the perceiving surface of the cell. A axon of the nervous cell forms synaptic connections with other neurons or with effector cells. Nervous impulse is always distributed in one direction: according to dendrites to the cell body, according to axon - from the body of the cell (the law of dynamic polarization of the Ramon-Ikakhal nervous cell). As a rule, neuron has many "inputs" carried out by dendrites, and only one "output" (axon) (see Fig. 1.3).
Neurons communicate with each other using the potentials of action that apply to axon. Potentials of the action comes from one neuron to the following as a result of synaptic transmission. The action potential that has reached the presynaptic ending is typically launches the release of the neurotiator, which either excites the postsynaptic cell, so that it arises in it from one or more of the action potentials, or inhibits its activity. Aksona not only transmit information in nervous
Fig. 1.3.The structure of the neuron. BUT- Typical neuron, consisting of the actual body, dendrites and axon: 1 - the beginning of the axon; 2 - dendrites; 3 - neuron body; 4 - axon; 5 - Schwann cell; 6 - axon branching. B.- Increased neuron body. The axonal holmik does not contain the substances of Nissla: 7 - core; 8 - Golgi devices; 9 - mitochondria; 10 - axonal holloch; 11 - Nissl Substance
chains, but also deliver by axon transport Chemicals to synaptic endings.
There are numerous classifications of neurons in accordance with the form of their body, the length and form of dendrites and other signs (Fig. 1.4). According to the functional value, the nerve cells are divided into afferent (sensitive, sensory), delivering pulses to the center, efferent (motor, motor), carrying information from the center to the periphery, and insert (insertions), in which pulses are recycling and collateral communications are organized.
The nerve cell performs two main functions: specific processing of incoming information and the transmission of the nerve impulse and biosynthetic, aimed at maintaining its livelihoods. It finds an expression in the ultrastructure of the nervous cell. Transferring information from one nervous cell to another, the union of nerve cells into the system and complexes of various complexity are carried out by the neuron structures: axon, dendrites and synapses. Organelles associated with the provision of energy exchange, the cells of the cells, occur in most cells; In the nervous cells, they perform the functions of energy supply, processing and transmission of information (see Fig. 1.3).
Neuron structure. Soma.The body of the nervous cell has a rounded or oval shape, in the center (or slightly eccentric) is the kernel. It contains nucleoline and surrounded by outer and internal nuclear membranes with a thickness of about 70 ǻ each, separated periods
Fig. 1.4.Variants of neurons of different shapes.
BUT- PseudoNipolar Neuron. B.- Purkinier cell (dendrites, axon). AT- Pyramid cell (axon). G.- Motioneron Front Horn (Akson)
nuclear space, the dimensions of which are variable. Chromatin's chromatin is divided into citioplasm, localized mainly in the inner nuclear membrane. In the cytoplasm of nerve cells there are elements of a grainy and non-critical cytoplasmatic network, polysomes, ribosomes, mitochondria, lysosomes, multi-public tanks and other organelles (Fig. 1.5).
The neuron's biosynthesis apparatus includes the Nissl Taurus - tightly adjacent flexible tanks of the granular endoplasmic reticulum, as well as a well-pronounced Golgi apparatus. In addition, catfish contains numerous mitochondria, which determine its energy exchange, and elements of the cytoskeleton, including neurofilaments and microtubule. Lizosomes and Fagosomas are the main organhellary of the "intracellular digestive tract".
Dendriti.Dendriti and their branching determine the receptive field of one or another cell (see Fig. 1.5). With an electron microscopic study, it is found that the neuron body is gradually moving into dendrites. The sharp boundaries and pronounced differences in the ultrastructure of the Soma and the initial department of large dendrites are not observed. Dendriti are very variable in shape, magnitude, branching and ultrastructure. Usually several dendrites are departed from the body. The length of the dendrite may exceed 1 mm, their share accounts for more than 90% of the surface area of \u200b\u200bthe neuron.
The main components of the cytoplasm of dendrites are microtubules and neurofilaments; In the proximal parts of dendrites (closer to the cellular body) contains the Nissl Taurus and the plots of the Golgi apparatus. Earlier it was believed that dendrites are electrically non-demanded, it is currently proven that dendrites of many
Fig. 1.5.Ultrastructure nervous cell.
1 - core; 2 - granular endoplasmic network; 3 - Plate complex (Golgi); 4 - mitochondria; 5 - lysosomes; 6 - Multivaicular body; 7 - Polisomas
neurons have potential-dependent conductivity, which is due to the presence of calcium channels on their membranes, when activated which the action potentials are generated.
Akson.Axon takes the beginning of the axon hilly - a specialized area of \u200b\u200bthe cell (more often than the Soma, but sometimes - dendrite) (see Fig. 1.3). Axon and Aksonny Khlomik differ from the soma and proximal sections of dendrites. The absence of a granular endoplasmic reticulum, free ribosomes and a Golgi apparatus. There are smooth endoplasmic reticulum and a pronounced cytoskeleton in the aston.
Axons are coated with myelin shell, forming myelin fibers. Bunches of fibers (in which there may be separate non-moving fibers) make up a white brain substance, cranial and peripheral nerves. When the axon is transition to the presynaptic ending, filled with synaptic bubbles, the axon forms a flask-shaped expansion.
The interlacing axons, dendrites and the process of glial cells create complex, non-repeating pictures of neuropil. Distribution of axons and dendrites, their interposition, afferent-effortive relationships, the patterns of synapotoarchitectonics determine the mechanisms of the integrative function of the brain.
Types of neurons.The polymorphism of the structure of neurons is determined by their different role in the system of brain as a whole. Thus, the neurons of the ganglia rear roots of the spinal cord (spinal ganglia) receive information not by synaptic transmission, but from sensory nerve endings in receptor organs. In accordance with this, cellular bodies of these neurons are devoid of dendrites and do not receive synaptic endings (bipolar cells; Fig. 1.6). Coming out of the cell body, the axon of such a neuron is divided into two branches, one of which (peripheral proceedings) is sent in the composition of the peripheral nerve to the receptor, and the other branch (central process) enters the spinal cord (as part of the rear root) or in the brain barrel ( As part of the cranial nerve). Neurons of another type, such as the pyramidal cells of the cortex of large hemispheres and the ceremonic cerebission cells, are occupied by processing information. Their dendrites are covered with dendritic spines and have an extensive surface; It comes to a huge amount of synaptic inputs (multipolar cells; see Fig. 1.4, 1.6). You can classify neurons along the length of their axons. Neurons of the 1st type of Golgji Aksonos are short, ending, as well as dendrites, close to the som. Type 2 neurons have long axons, sometimes longer than 1 m.
Neuroglia
Another group of cell elements of the nervous system is neuroglia (Fig. 1.7). In the CNS of a person, the number of neuroglial cells is an order of magnitude greater than the number of neurons: 10 13 and 10 12, respectively. Close morphological relationship is the basis for the physiological and pathological interactions of Glia and Neurons. Their relationship is described by the concept of dynamic neuronal-glial signal processes. The possibility of transmitting signals from neurons to the Glia and, thus, to other neurons opens up many options for intercellular "cross-conversations".
There are several types of neuroglia, in the Central CNS neuroglia is represented by astrocytes and oligodendrocytes, and in PNS - Schwannovsky cells and satellite cells. In addition, microglia cells and ependym cells are considered central glial cells.
Astrocytes.(called the name due to its star form) regulate the condition of the microenvironment around the TSS neurons. Their processes are surrounded by groups of synaptic endings, which are as a result isolated from neighboring synapses. Special processes - "legs" of astrocytes form contacts with capillaries and connective tissue on the surface of the head and spinal cord (soft cerebral shell) (Fig. 1.8). The legs limit the free diffusion of substances in the CNS. Astrocytes can actively absorb to + and neurotransmitters, then metabolizing them. Due to the selectively increased permeability for ions K + Astrogenia regulates the activation of the enzymes necessary to maintain the metabolism of neurons, as well as to remove mediators and other agents that are distinguished by neuro-
Fig. 1.6.The classification of neurons by the number of processes derived from the body of the cell.
BUT -bipolar. B.- PseudoNechnipolar. AT- Multipolar. 1 - dendrites; 2 - Akson
Fig. 1.7.The main types of glial cells.
BUT- Protoplasic astrocyte. B.- Microglyal cell. AT- Oligrordrocyte. G.- Fibrous Astrosite
nal activity. Astrogenia is involved in the synthesis of immune mediators: cytokines, other signal molecules (cyclic guanosine monophosphate - sommnitrogen oxide - NO), then transmitted to neurons - in the synthesis of glial growth factors ( GDNF),participating in trophic and reparation neurons. Astrocytes are capable of reacting to an increase in the synaptic concentration of neurotransmitters and the change in the electrical activity of neurons by changes in the intracellular concentration of Ca 2+. This creates a "wave" of Ca 2+ migration between astrocytes capable of modulating the state of many neurons.
Thus, astrohlo, not only the trophic component of the nervous system, is involved in the specific functioning of nervous tissue. In the cytoplasm of astrocytes there are clay filaments performing mechanical reference function in the TSN tissue. In the event of damage to the process of astrocytes containing clay filaments, hypertrophy is subjected and form a glilatic scar.
The main function oligodendrocyteit is the provision of electrical insulation of axons by forming a myelin shell (Fig. 1.9). This is a multi-layer wrapper, spirally wound over the plasma stammes of axons. In the PNS, myelin shell is formed by the membranes of Schwann cells (see Fig. 1.18). Melin represents
the packaging of sheets of specific plasma membranes rich in phospholipids, and also contains proteins of several types, various in the central nervous system and PNS. Protein structures allow plasma membranes tightly packaging together. With the growth of the glyonic cell membrane, it occurs around the neuron axon with the formation of a layered spiral with a double plasma membrane around the axon. The thickness of the myelin shell can be 50-100 membranes playing the role of an axon's electric insonator, which prevents ion exchange between the axon cytozem and the extracellular medium.
In addition, the composition of neuroglia includes satellite cells that encapsulate the neurons of ganglia spinal and cranial nerves, adjusting the microenide around these neurons like the astrocytes (Fig. 1.10).
Another kind of cells - microgliaor latent phagocytes. Microglia is the only representation of immunocompetent cells in the central nervous. It is widely represented in the entire human brain tissue and is 9-12% of the total global population in the gray matter and 7.5-9% in the white substance. In contrast to astrocytes, microglyal cells occur from stem cells and in normal conditions have vehicles
Fig. 1.8.The interaction of astrocytes with the surrounding cellular elements.
1 - Tainicit; 2 - the cavity of the ventricle; 3 - ependimal cells; 4 - capillary; 5 - neuron; 6 - myelinated axon; 7 - soft brain shell; 8 - Subarachnoid space.
The figure shows two astrocytes and their relationship with ependymal cells, lining ventricles, pericarion, dendrites of neuron, capillary, as well as flat epithelium soft cerebral shell. It should be noted that this pattern is schematically schematically and the connection of neuron simultaneously with the ventricle and the subarachnoid space is unlikely
Fig. 1.9.Oligodendrocyte: the formation of an Akson myelin shell. 1 - axon; 2 - myelin; 3 - smooth endoplasmic reticulum; 4 - neurofilaments; 5 - Mitochondria
Fig. 1.10.The interaction of glial cells and neurons. Schematically depicted arrows. 1 - satellite clay cell; 2 - clay cell, synthesizing myelin
wasty shape with a variety of processes. The activation of microglia, in particular in hypoxia conditions, is accompanied by products of pro-inflammatory mediators with toxic properties. The chronic inflammatory response in the brain tissue leads to the delayed neuronal losses, microcirculatory disorders, changes in the function of the hematorencephalic barrier.
In pathological conditions, microglyal cells draw the processes and take an amoeboid form, which corresponds to their pronounced functional activation up to the state of phagocytosis. In case of damage to the brain tissue, the microgelia along with penetrating the CNS from the blood flow phagocytes contributes to the removal of cellular decay products.
The TSNS tissue is separated from the cerebrospinal fluid (CSW), filling the ventricle of the brain, the epithelium, which is formed by ependymal cells. Ependim provides diffusion of many substances between the extracellular space of the brain and the CES. CSH secrete specialized ependymal cells of vascular plexuses in the ventricular system.
Admission to the cells of the brain of nutrients and the removal of the products of the vital activity of the cells occur through the vascular
system. Although the nervous tissue is replete with capillaries and other blood vessels, the hemat and belated barrier (GEB) limits the diffusion of many substances between the blood and the TSN fabric.
1.3. Electrical transmission of information between neurons
The normal activity of the nervous system depends on the excitability of its neurons. Excitability- This is the ability of cell membranes to respond to the effect of adequate irritants with specific changes in ionic conductivity and membrane potential. Excitation- an electrochemical process that comes exclusively on the cytoplasmic membrane of the cell and characterized by changes in its electrical state, which starts the function specific for each tissue. Thus, the excitation of the muscle membrane causes its abbreviation, and the excitation of the neuron membrane is to carry out an electrical signal on axon. Neurons have not only potential-controlled, i.e. Adjustable electrical pathogens ion channels, but also chem controlled and mechanically controlled.
There are differences in the relationship between the membrane potential / permeability of the membrane and the type of stimulus. When exposed to an electric stimulus, the event chain is as follows: irritant (electric current) \u003d\u003e Shear of the membrane potential (to critical potential) \u003d\u003e Activation of potential-controlled ion channels \u003d\u003e Changes in the ion permeability of the membrane \u003d\u003e Changes in ionic currents through the membrane \u003d\u003e Further shift of the membrane potential (the formation of the action potential).
When exposed to a chemical stimulus, a fundamentally different chain of events occurs: stimulus (chemical) \u003d\u003e chemical binding of the stimulus and receptor of the chem controlled ion channel \u003d\u003e Change the conformation of the ligandrechette complex and the opening of the recipe-controlled (chem controlled) ion channels \u003d\u003e Change the ion permeability of the membrane \u003d\u003e Change the ionic currents through the membrane \u003d\u003e membrane potential shift (formation, For example, local potential).
The chain of events under the influence of a mechanical stimulus is similar to the previous one, as in this case the recipes are also activated
rights ion channels: irritant (mechanical stress) \u003d\u003e change in the membrane tension \u003d\u003e Opening of recipe-controlled (mechanically controlled) ion channels \u003d\u003e Change the ion permeability of the membrane \u003d\u003e Changes in ionic currents through the membrane \u003d\u003e The shear of the membrane potential (the formation of mechanicalinduced potential).
Passive electrical properties of the cell are associated with the electrical properties of its membrane, cytoplasm and the external environment. The electrical properties of the cell membrane are determined by its capacitive and resistive characteristics, since the lipid bilayer is really able to easily be condenser, and the resistor. The capacitive characteristics of the lipid bilayer and the real membrane are similar, and the resistive varies due to the presence of primarily proteins forming ion channels. In most cells, the input resistance behaves nonlinearly: for the current flowing in one direction, it is greater than for the opposite direction. This property of asymmetry reflects an active reaction and is called straightening. The current flowing through the membrane is determined by the capacitive and resistive components. The resistive component describes the actual ion current, since electricity is transferred in the cell by ions. The movement of ions into a cell or from a cell is hampered by plasma membrane. Since the membrane represents a lipid bilayer, impenetrable for ions, it has resistance. On the contrary, the membrane has some conductivity for ions that pass through ion channels. Due to the obstacles to the free movement of ions outside and inside the cell there are identical ions, but at different concentrations.
There are two fundamental mechanism for moving substances through the membrane - by simply diffusion (Fig. 1.11) and when
Fig. 1.11.Transportation of substances through the cell membrane.
BUT- Simple diffusion. B.- Light diffusion. AT- Active transport: 1- membrane
the relics of specific carriers embedded in the membrane and represent transmembrane integral proteins. The latter mechanism includes lightweight diffusion and active ion transport, which can be primary active and secondary-active.
Through a simple diffusion (without the help of the carrier), vehicles can be transported by water-soluble organic compounds and gases (oxygen and carbon dioxide) through lipid bilayer by dissolving in the lipids of the cell membrane; Na +, Ca 2+, K +, Cl - via ionic channels of the cell membrane connecting the cytoplasm of cells with an external medium (passive ion transport, which is determined by an electrochemical gradient and is directed from greater electrochemical potential to a smaller: inward cells for Na + ions, CA 2+, CL -, outward - for ions to +); Water molecules through the membrane (osmosis).
With the help of specific carriers, an energetically independent lightweight diffusion of a number of compounds is carried out (see Fig. 1.11). A bright example of lightweight diffusion is glucose transport through a neuron membrane. Without a specialized astrocytic carrier, the admission of glucose in neurons would be almost impossible, as it is a relatively large polar molecule. Due to its rapid transformation into glucose-6-phosphate, the intracellular glucose level is lower than extracellular level, and thus the gradient is preserved, providing a continuous glucose flow into neurons.
Energy dependent primary-active transport ions Na +, Ca 2 +, K +, and H + is an energy-dependent transfer of substances against their electrochemical gradients (see Fig. 1.11). Due to it, the cells can accumulate ions in concentrations, higher compared to the environment. Movement from lower to a higher concentration and maintenance of the steady gradient is possible only with continuous energy supply of the transport process. With primary active transport, direct consumption of ATP occurs. ATP-energy pumps (ATPase) transport ions against their concentration gradient. Based on the peculiarities of the molecular organization, 3 grams are distinguished - p, v and f (Fig. 1.12). All three classes of atfas have one or more places of binding to ATP on the cytosolic surface of the membrane. The class p includes C C 2+ -ATPAZ and Na + / K + -ATFAZ. Carriers of active ion transport are specific for the transported substance and saturated, i.e. Their flow is maximum when all specific binding places with a tolerated substance are busy.
Many gradients of the electrochemical potential of the cell, which are a prerequisite for passive ion transfer, appear as a result of their active transport. Thus, the gradients K + and Na + arise as a result of their active transfer Na + / K + - pump (Fig. 1.13). Due to the activity of Na + / K +-turns inside the ion cells, K + are present in a higher concentration, but they strive through diffusion to switch to the extracellular medium to the concentration gradient. To preserve the equality of positive and negative charges inside the cell, the output into the ion ion environment should be compensated by the inlet of the Na + ion cell. Since the membrane alone is much less permeable for Na + ions than for ions K +, potassium should leave the cell on the concentration gradient. As a result, a positive charge is accumulated on the outside of the membrane, and on the inner - negative. This is supported by the potential of rest of the membrane.
The secondary-active transport of a number of ions and molecules also uses energy accumulated as a result of ATP consumption and spent on the creation of a concentration gradient. The ion concentration gradient relative to the membrane is used as an energy source created by primary active transport (Fig. 1.14). Thus, the secondary-active transport includes the battry and anti-transport: the flow of ions from a higher (higher energy state) to a lower (lower energy state) of the concentration provides energy to move the actively transportable substance from its low concentration area to the high area.
Fig. 1.12.Three grades of ATP-dependent ion pumps. BUT- P-class. B.- F 1 class AT- V 1-class
Cell potentials determined by passive ion transport
In response to a subgrown, close to the threshold and threshold pulses of an electric current, there are respectively passive electrotonic potential, a local response and potential of action (Fig. 1.15). All these potentials are determined by passive ion transport through the membrane. For their occurrence, the polarization of the cell membrane is required, which can be carried out extracellularly (usually observed on nerve fibers) and intracellularly (usually marked on the body of the cell).
Passive electrotonic potentialit occurs in response to the sub-step impulse, which does not lead to the discovery of ion channels and is determined only by the capacitive and resistive properties of the cell membrane. Passive electrotonic potential is characterized by a time constant, which reflects the passive properties of the membrane of the temporary course of changes in the membrane potential, i.e. The speed with which it changes during the transition from one value to another. Pass-
Fig. 1.13.NA + / K + pumping mechanism
Fig. 1.14.The mechanism of operation of secondary-active transport. BUT- Stage 1. B.- Stage 2. AT- Stage 3: 1 - Na +; 2 - a substance molecule that must be moved against the concentration gradient; 3 - conveyor. Under the binding of Na + with a carrier, altoherectural changes arise in the binding center of the carrier protein for the portable molecule, which causes conformational changes to the carrier protein that allow Na + ions and the associated substance to exit the other side of the membrane
the powerful electrotonic potential is inherent in the equality of rapid rates and a decline of exhibitors. There is a linear relationship between the amplitudes of the electric stimulus and the passive electrotonic potential, and the increase in the duration of the pulse does not change this pattern. Passive electrotonic potential applies to axon with attenuation, which is determined by the constant length of the membrane.
With the approach of the power of the electrical pulse to the threshold occurs local response membrane,which is manifested by a change in the form of passive electrotonic potential and the development of an independent peak of a small amplitude, in the form of a resembling S-shaped curve (see Fig. 1.15). The first signs of local response are recorded under the action of incentives that make up about 75% of the threshold value. When the irritant current amplitude is increased, the local response increases nonlinearly and can not only reach the critical potential, but also exceed it, not interpretable, however, into the action potential. An independent development of a local response is associated with an increase in the sodium permeability of the membrane through sodium channels that provide an incoming current, which in the threshold irritant causes the depolarization phase of the action potential. However, with a sub-stimulus, this increase in permeability is not enough to launch the process of regenerative depolarization of the membrane, since only a small part of sodium channels opens. Started
Fig. 1.15.Cell membrane potentials.
BUT- Dynamics of changes in the membrane potential, depending on the force of the depolarizing pulse of the electric current. B.- Discrete increase in the force of depolarizing pulse
polarization is suspended. As a result of the exit from the ion cell, the potential is returned to the level of rest potential. In contrast to the action potential, the local answer does not have a clear threshold of occurrence and does not obey the law "All or Nothing": with an increase in the power of the electric impulse of the local answer amplitude. In the body, a local response is an electrophysiological expression of local arousal and, as a rule, precedes the potential of action. Sometimes the local answer may exist independently in the form of an exciting postsynaptic potential. Examples of the independent value of the local potential are the excitation of the NETON-neuron-neurons, devoid of axons, devoid of axons, to synaptic endings, as well as the response of the postsynaptic chemical synapse membrane and the communicative transmission of information between the nervous cells generating synaptic potentials.
With the threshold value of an irritating electrical impulse arises action potentialconsisting of depolarization and repolarization phases (Fig. 1.16). The potential of action begins as a result of the displacement under the action of a rectangular pulse of the electric current of the rest potential (for example, from -90 mV) to the level of critical potential (different for cells of various types). The depolarization phase is based on the activation of all potentially controlled sodium channels, after
Fig. 1.16.Changes in the membrane potential of the neuron (BUT)and the conductivity of ions through plasmolemma (B)if the potential occurs. 1 - Fast depolarization; 2 - overrun; 3 - Repolarization; 4 - threshold potential; 5 - hyperpolarization; 6 - rest potential; 7 - Slow depolarization; 8 - action potential; 9 - permeability for sodium ions; 10 - permeability for potassium ions.
The conductivity curves of ions are interconnected with the action potential curve
what the passive transport of Na + ions is increasing inside the cell and the displacement of the membrane potential of up to 35 mV arises (this peak level is different for cells of different types). Exceeding the potential of the values \u200b\u200bover the zero line is called an overwhelm. Upon reaching the peak, the magnitude of the potential falls into the negative area, reaching the resting potential (repolarization phase). The basis of repolarization is the inactivation of potentially controlled sodium channels and the activation of potentially controlled potassium channels. The ions to + passive transport overlook the cell and the current occurrence leads to the displacement of the membrane potential into the negative area. The repolarization phase is completed by trace hyperpolarization or trace depolarization - alternative ion mechanisms for the return of the membrane potential at the level of rest potential (see Fig. 1.16). At the first mechanism, repolarization reaches the quantity of rest and continues further into a more negative area, after which it returns to the level of rest potential (trace hyperpolarization); With a second - repolarization occurs slowly and smoothly passes into resting potential (trace depolarization). The development of the potential of the action is accompanied by phase changes in cell excitability - from increased excitability to absolute and relative refractoriness.
Bioelectric activity of neurons
The first type of cell bioelectric activity is inherent in silent neurons, which cannot independently generate the action potentials. The potential of resting these cells does not change (Fig. 1.17).
Second-type neurons are able to independently generate the action potentials. Among them, cells that generate a regular and irregular rhythmic or pack (a package of several potentials of action is distinguished, after which a short period of rest is observed) activity.
The third type of bioelectric activity includes neurons that can independently generate fluctuations of the rest potential of a sinusoidal or saw-shaped form that do not reach critical potential. Only rare oscillations can reach the threshold and cause the generation of single action potentials. These neurons were called Paissener (Fig. 1.17).
The "behavior" of individual neurons and internecronal interactions are influenced by long-term polarization (depolarization or hyperpolarization) of postsynaptic cell membranes.
Stimulation of neurons by constant depolarizing electric shock causes answers by rhythmic discharges of action potentials. After the cessation of long-term depolarization, the membrane comes automatic braking,in which the cell is not able to generate the potentials of the action. The duration of the stage of the coming braking is directly correlated with the amplitude of the stimulating current. The cell then gradually restores the usual rhythm of the generation of potentials.
On the contrary, the permanent hyperpolarizing current inhibits the development of the action potential, which is of particular importance in relation to neurons with spontaneous activity. The increase in the hyperpolarization of the cell membrane leads to a decrease in the frequency of spike activity and an increase in the amplitude of each action potential; The next stage is the complete cessation of potential generation. After the cessation of long-term hyperpolarization, the membrane comes the phase post-yard activation,when the cell begins to spontaneously generate with a higher frequency than usual, the potentials of the action. The duration of the response activation step directly correlates with the amplitude of the hyperpolarizing current, after which the cell gradually restores the usual rhythm of the generation of potentials.
Fig. 1.17.Types of bioelectric activity of nerve cells
1.4. Conducting nervous fiber
The patterns of carrying out the excitation of nervous fibers are defined by both electrical and morphological features of axons. Nervous trunks consist of myelinized and non-cellinized fibers. The membrane of a nonimeelainized nervous fiber is directly in contact with the external environment, i.e. The exchange of ions between the intracellular and extracellular medium can occur at any point of non-moving fiber. The myelinated nerve fiber is covered with fatty (myelin) shell that performs the function of the insulator (see Fig. 1.18).
Myelin from one global cell forms a deelinated nerve fiber region, separated from the next region formed by another clay cell, a non-aelainized area - in the interception of Ranvier (Fig. 1.19). The length of the interception of Ranvier is only 2 microns, and the length of the myelinized fiber section between the adjacent interceptions of Ranvier reaches 2000 microns. Interceptions of Ranvier are completely free from myelin and can be in contact with extracellular fluid, i.e. The electrical activity of myelinized nerve fibers is limited to the membrane of interception Ranviers, through which ions are capable of penetrating. In these areas, the membrane marks the greatest density of potential-controlled sodium channels.
Passive electrotonic potential spreads through the nerve fiber for small distances (Fig. 1.20), while its amplitude
Fig. 1.18.Moneelination diagram of peripheral nervous fiber. BUT- Stages of myelinization. A - Axon worst with a process of Schwannovsky cell; b - the process of Schwannskoy cell winds around the axon; In - Schwannskaya cell loses most of the cytoplasm, turning into a plate shell around the axon. B.- Nevilinized axons, surrounded by the process of Schwannsky cell
Fig. 1.19.The structure of the interception of Ranvier.
1 - plasma membrane axon;
2 - myelin membranes; 3 - cytosol of the Schwann cell; 4 - Ranvier interception zone; 5 - Plasma membrane of Schvanna cell
there, the rate of increase and falling with distance decrease (the attenuation phenomenon of the excitation). The propagation of excitation in the form of the potential of action is not accompanied by a change in the shape or amplitude of the potential, since the potential-controlled ion channels are activated in the threshold depolarization, which does not occur when the passive electrotonic potential is distributed. The process of propagation of the action potential depends on passive (capacity, resistance) and active (activation of potential-controlled channels) of the properties of the neural fiber membrane.
And the inner, and the outer environment of the axon is a good conductor. The axon membrane, despite the insulating properties, can also carry out the current due to the presence of the "leakage" channels. In case of irritation of the non-moving fiber at the irritation site, potentially controlled sodium channels open, which causes the occurrence of the incoming current and the generation of the depolarization phase of the action potential on this area of \u200b\u200bthe axon. The incoming current Na + induces local circles of the current between depolarized and nonpolarized regions of the membrane. Thanks to the mechanism described in non-cellinized fiber, the action potential applies to both sides of the excitation site.
In myelinized nerve fiber, the potentials of the action are generated only in the interceptions of Ranvier. The electrical resistance of sections covered with myelin shell high and does not allow the development of local circular currents that are necessary to generate the potential of action. When the excitation of the arhelinized fiber is spreading, the nervous impulse jumps from one interception of Ranvier to another (s) (see Fig. 1.20). In this case, the potential of action may be distributed in both directions from the place of irritation, as in the non-cellinized fiber. Saluator
Fig. 1.20.The distribution scheme of the electric potential on the nervous fiber.
A.- Distribution of the potential of actions for a non-family axon: A - Akson alone; b - initiation of the potential of the action and the occurrence of local currents; in - the distribution of local currents; D - Distribution of Axon's action potential. B.- Distribution of the action potential from the neuron body to the terminal end. B.- Saltor conducting impulse on myelinized fiber. Interceptions of Ranviers share the segments of the Micheeline Shell axon
the pulse provides 5-50 times the highest speed of excitation compared to non-cellinized fiber. In addition, it is more economical, since the local depolarization of the axon membrane only in the place of interception of Ranvier leads to a loss of 100 times less ions than when forming local currents in non-cellinized fiber. In addition, the potentially controlled potential channels are minimally involved, as a result of which the potentials of the myelinized fibers often do not have a phase of trace hyperpolarization.
The laws of excitation on the nervous fiber First Law:when irritating the nervous fiber, the excitation of the nerve spreads in both directions.
Second Law:the spread of excitation in both directions occurs at the same speed.
Third Law:the excitation of the nerve spreads without phenomenon attenuation, or without a decrement. Fourth Law:conducting the excitation of nervous fiber is possible only with its anatomical and physiological integrity. Any injury of the surface membrane of the nerve fiber (cut, compression due to inflammation and edema of the surrounding tissues) disrupts irritation. Conducting is violated and when changing the physiological status of the fiber: the blockade of ion channels, cooling, etc.
Fifth Law:excitement of nervous fibers is isolated, i.e. It does not switch from one fiber to another, and excites only those cells with which the endings of this nervous fiber contact. Due to the fact that the composition of the peripheral nerve usually includes many different fibers (motors, sensitive, vegetative), innervating different organs and tissues and performing different functions, isolated on each fiber is of particular importance.
Sixth law:nervous fiber is not tired; The potential of the fiber action has the same amplitude for a very long time.
Seventh Law:the rate of excitation is different in different nerve fibers and is determined by the electrical resistance of the intra-and extracellular medium, the axon membrane, as well as the diameter of the nerve fiber. With an increase in the fiber diameter, the rate of irritation increases.
Classification of nerve fibers
Based on the rate of excitation by nerve fibers, the duration of the phases of the potential of action and the characteristics of the structure, three main types of nerve fibers are distinguished: A, B and C.
All fibers of type A amelinated; They are separated by 4 subgroups: α, β, γ and δ. The largest diameter of α-fibers (12-22 μm), which determines the high speed of excitation on them (70-170 m / s). The fibers of the type αa in humans are excited from the motor neurons of the front horns of the spinal cord to skeletal muscles, as well as on the propriceceptive muscle receptors to the Sensitive CNS centers.
Other fibers type A.(β, γ and δ) have a smaller diameter, less excitation rate and a longer potential of action. These groups of fibers include mainly sensitive fibers, conductive pulses from various receptors in the central nervous system; The exception is the fibers Γa, which are excited from the γ-neurons of the front horns of the spinal cord to intraphus muscle fibers.
Fiber type B.also, myelinated, relating mainly to the pregganent fibers of the vegetative nervous system. The rate of conduct on them is 3-18 m / s, the duration of the action potential is almost 3 times higher than the similar indicator of type A. fibers for these fibers is not characterized by the trace depolarization phase.
Fiber type S.nevilinated, have a small diameter (about 1 μm) and low excitation rate (up to 3 m / s). Most type C fibers are postganglyonic fibers of the sympathetic nervous system, some type fibers are involved in excitation from pain, temperature and other receptors.
1.5. Coding
Information transmitted by axon in one way or another is encoded. A combination of neurons providing a specific function (for example, a specific sensor modality) generates a projection path (the first coding method). So, the visual path includes the neurons of the retina, the lateral crankshaft of the thalamus and the visual areas of the crust of large hemispheres. Axons, conductive visual signals, are part of the optic nerve, the visual path, visual radiation. The physiological incentive to activate the visual system is the light falling on the retina. Retinal neurons convert this information and transmit a signal further by the visual path. However, with mechanical or electrical irritation of the neurons of the visual path, the visual sensation also arises, although, as a rule, is distorted. So, the neurons of the visual system make up the projection path, when activated which the visual sensation arises. Motor tracks also represent projection structures. For example, when you activate certain neurons of large semi-corthesis, discharges are generated in the muscles of the muscles of the brush, and these muscles are reduced.
The second coding method is due to the principle of an ordered spatial (somatotopic) CNS organization. Somatotopic maps are compiled by certain groups of neurons of sensory and motor systems. These groups of neurons, firstly, receive information from the appropriately localized areas of the body surface and, secondly, send motor commands to certain parts of the body. In the visual system, the retina sections are presented in the core of the brain with groups of neurons forming retinotopic maps. In the auditory system, the frequency response sounds are reflected in the tunication cards.
The third method of encoding information is based on varying the characteristics of the sequences (series) of the nerve impulses,
as a result of synaptic transmission to the next group of neurons, while the coding mechanism is the temporary organization of the discharge of nerve impulses. Different types of such coding are possible. Often the code is the average frequency of discharge: in many sensory systems, an increase in the intensity of the intensity is accompanied by an increase in the frequency of discharge of sensory neurons. In addition, the code can be the duration of the discharge, a variety of pulse grouping in the discharge, the duration of high-frequency losses of pulses, etc.
1.6. Conducting excitation between cells.
The relationship between nerve cells is carried out by internecronal contacts, or synapses. Information in the form of a series of action potentials comes from the first (presynaptic) neuron to the second (postsynaptic) or by forming a local current between adjacent cells (electrical synapses), or indirectly by chemicals - mediators, neurotransmitters (chemical synapses), or using both mechanisms ( Mixed synapses). Fast signal transmission is carried out by electrical synapses, slower - chemical.
Typical synapses are the formation formed by the terminals of the axon of one neuron and dendrites of the other (accelendritic synapses). In addition, there are axomatic, ax and axonal and dendrodritic synapses (Fig. 1.21). Some associative neurons have a variety of synaptic ties (Fig. 1.22). Sinaps between the motor mechanone axon and the fiber skeletal muscle is called a motor end plate, or a nervous compound.
W. electric synapsa(Fig. 1.23) Cell membranes of neighboring neurons are closely adjacent to each other, the slot between them is about 2 nm. The sembranes of neighboring cells that form a slit contact contain specific protein complexes consisting of 6 subunits (connects) located in such a manner that in the center of the contact form a water filled. Connexon membranes of neighboring cells, lining against each other, form an open connection - "Channels", the distance between which is about 8 nm.
Fig. 1.21.The main types of synapses.
BUT- A - electrical synaps; b - spichy synaps containing electron-dense vesicles; at - "ENpassant »Synaps, or synaptic" kidney "; M - brake synaps, located on the initial part of the axon (contains ellipsoid vesicles); d - dendritic spike; E - Shipic synaps; f - brake synaps; z - axer-axonal synaps; and - reciprocal synaps; K is an exciting synaps. B.- Nepical synapses: 1 - Aksco-axonal synaps. The end of one axon can adjust the activity of another; 2 - Dendrodrich Synaps; 3 - somdom synaps
Electrical synapses are most often formed in the embryonic stage of development, in adult their number decreases. However, in an adult body, the significance of electrical synapses is preserved for the cells of the glill and the amacrine retinal cells; Electrical synapses can be detected in the brain barrel, especially in the lower olives, in the retina of the eye, vestibular roots.
Depolarization of the presynaptic membrane leads to the formation of the difference in potentials with a non-compolarized postsynaptic membrane. As a result, through the channels formed by Connekes, the movement of positive ions on the gradient of the potential difference in the postsynaptic cell or the movement of anions in the opposite direction. Upon reaching the postsynaptic membrane
Fig. 1.22.Associative neuron with multiple synaptic connections.
1 - Akson Kholmik, turning into Akson; 2 - Melinic shell; 3 - accelendritic synaps; 4 - core; 5 - dendrite; 6 - Acosomatic synaps
Fig. 1.23.The structure of electrical synapse.
BUT- Slitel contact between the sembran areas of neighboring cells. B.- Connexon membranes of neighboring cells form an interneurone "channel". 1 - protein complex; 2 - ion channel. 3 - channel; 4 - Connexon cell 1; 5 - every six subunits; 6 - Connexon Cell 2
the total depolarization of the threshold value occurs the potential of action. It is important to note that in electrical synapse, ionic currents arise with a minimal time delay of 10 -5 C, which explains the high synchronization of the response even a very large number of cells connected by slotted contact. Conducting current through electrical synaps is also possible in both directions (as opposed to chemical synapse).
The functional state of electrical synapses is regulated by ions Ca 2+ and the level of the membrane cell potential, which creates conditions for the effect on the spread of excitation, up to its termination. The peculiarities of the activities of electrical synapses include the impossibility of direct transfer of excitation to remote cells, since only a few others are associated with an excited cell; The level of excitation in the presynaptic and postsynaptic cells is the same; Burn the spread
the excitation is impossible, in connection with this brain of newborns and young children, containing significantly more electrical synapses than the adult brain, it turns out to be much more excited for electrical processes: the rapidly propagating electrical excitation is not exposed to braking correction and almost instantly becomes generalized, which explains it. Special vulnerability and exposure to the development of paroxysmal activity.
It should be noted that in some forms of demyelinizing polyneuropathies axons, which are part of one nervous barrel, begin to closely touch each other, forming pathological zones (efaps), within which it becomes possible to "jump over" the action potential from one axon to another. As a result, the appearance of symptoms reflecting the admission of "pseudo-information" in the brain is possible - a feeling of pain without irritation of peripheral pain receptors, etc.
Chemical synapsalso transmits an electrical signal from the presynaptic to the postsynaptic cell, but in it, the ionic channels on the postsynaptic membrane open or closed using chemical substances-carriers (mediators, neurotransmitters) released from the presynaptic membrane (Fig. 1.24). Changing the possibility of conducting certain ions through the postsynaptic membrane is the basis of the functioning of chemical synapses. Ion currents change the potential of the postsynaptic membrane, i.e. cause the development of postsynaptic potential. Depending on whether the conductivity of which ions changes under the action of the neurotransmitter, its effect can be braking (hyperpolarization of the postsynaptic membrane due to the additional exit current of the ions K + or the incoming current of ions C1 -) or exciting (depolarization of the postsynaptic membrane with an additional incoming Ca 2+ ion current or Na +).
In synapse (Fig. 1.25), the presynaptic process, containing the presynaptic bubbles (vesicles), and the postsenptic part (dendrites, body of the cell or axon). In the presynaptic nervous ending in vesicles, neurotransmitters accumulate. The synaptic vesicles are fixed mainly on the cytoskeleton by means of proteins of synappsin, localized on the cytoplasmic surface of each vesicle, and spectrine located on the fiber of the cytoskeleton f-actin (Fig. 1.26). A smaller part of Vesikul is associated with presets
the supplied membrane by the protein of the vesicles of the Sinaptobrelevine and the protein of the presynaptic syntaxy membrane.
One vesicle contains 6000-8000 transmitter molecules, which is 1 kvant of transmitter, i.e. The minimum amount exempted into the synaptic gap. When a series of action potentials reaches a nervous end (presynaptic membrane), Ca 2+ ions are rushing inside the cell. On the vesicles associated with the presynaptic membrane, the ions of Ca 2+ are associated with the protein Vesikul Sinaptagmi-
Fig. 1.24.The main stages of transmission through the chemical synaps: 1 - the potential of action reaches the presynaptic end; 2 - depolarization of the presynaptic membrane leads to the discovery of potential-dependent Ca 2+ - channels; 3 - Ca 2+ ions mediate merge vesicles with a presynaptic membrane; 4 - the mediator molecules are released into the synaptic slit by exocytosis; 5 - the media molecules are associated with postsynaptic receptors, activating ion channels; 6 - a change in the conductivity of the membrane for ions is occurring and, depending on the properties of the mediator, an exciting (depolarization) or brake (hyperpolation) occurs (depolarization); the potential of the postsynaptic membrane; 7 - the ion current applies to the postsynaptic membrane; 8 - Mediator molecules are returned to the presynaptic ending by reverse capture or 9 - diffusted into extracellular liquid
mr. which causes the disclosure of the membrane vesicle (see Fig. 1.26). In parallel with this, the synaptophysine polypeptide complex merges with unidentified proteins of the presynaptic membrane, which leads to the formation of the pore, through which the adjustable exocytosis is carried out, i.e. The secretion of the neurotransmitter in the synaptic gap. Special proteins Vesicul (Rab3a) regulate this process.
SA 2+ ions in the presynaptic end are activated by CA 2+ -Calmodulin-dependent protein kinase II - an enzyme, phosphorylating synapsein on the presynaptic membrane. As a result, vesicles loaded by the transmitter can be free from the cytoskeleton and move to the presynaptic membrane for the implementation of the further cycle.
The width of the synaptic slit is about 20-50 nm. It is thrown into it the neurotransmitter molecules, the local concentration of which immediately after the emission is sufficiently high and is in the millimelar range. The neurotransmitter molecules diffuse to the postsynaptic membrane for about 0.1 ms.
In the postsynaptic membrane, the subsinaptic zone is isolated - the area of \u200b\u200bdirect contact of the presynaptic and postsynaptic membranes, also called the active zone of synapse. It is built into the proteins that form ion channels. At rest, these channels are rarely open. If the neurotransmitter molecules hit the postsynaptic membrane, they interact with the proteins of ion channels (synaptic receptors), changing their conformation and leading to a much more frequent opening of ion channels. Those receptors whose ion channels are opened with direct contact with the ligand (neurotransmitter) are called ionotropic.Receptors in which open
Fig. 1.25.The ultrastructure of the accelendritic synapse. 1 - axon; 2 - dendrite; 3 - mitochondria; 4 - synaptic bubbles; 5 - presynaptic membrane; 6 - postsynaptic membrane; 7 - synaptic gap
tie ion channels associated with the connection of other chemical processes, are called metabotropic(Fig. 1.27).
In many synapses, the neurotransmitter receptors are not only in postsynaptic, but also on the presynaptic membrane (Autorceptor).When the neurotransmitter interacts with the autoceptors of the presynaptic membrane, its release is enhanced or weakened (positive or negative feedback) depending on the type of synapse. The functional state of the deactors also affects the concentration of C 2+ ions.
Interacting with a postsynaptic receptor, neurotransmitter opens nonspicure ion channels in postsynaptic
Fig. 1.26.Docking vesicles in the presynaptic membrane. BUT- The synaptic vesicle joins the cytoskeleton element with a synappsin molecule. The docking complex is isolated by a quadrilateral: 1 - Samkinase 2; 2 - SINAPSIS 1; 3 - Fodrin; 4 - mediator carrier; 5 - synapotophysine; 6 - Docking Complement
B.- increased diagram of the docking complex: 7 - Sinaptobrevin; 8 - synapotoagmin; 9 - RAB3A; 10 - NSF; 11 - synapotophysine; 12 - Snap; 13 - syntaxin; 14 - neoskin; 15 - Fisophyllin; 16 - α-SNAP; 17 - CA 2+; 18 - N-sec1. Self-2 - calmodulin-dependent protein kinase 2; N-SECL - secretory protein; NSF - N-ethylmalemid-sensitive fusion protein; GAB3Z - GTFAZ from the RAS family; SNAP - Proshleptic membrane protein
membrane. Exciting postsynaptic potential arises due to an increase in the ability of ion channels to carry out monovalent cations depending on their electrochemical gradients. Thus, the potential of the postsynaptic membrane is in the range between -60 and -80 mV. The equilibrium potential for Na + ions is +55 mV, which explains the strong driving force for Na + ions inside the cell. The equilibrium potential for ions K + is approximately -90 mV, i.e. There is a slight current of ions K +, directed from the intracellular medium in extracellular one. The operation of ion channels leads to depolarization of the postsynaptic membrane, which is called exciting postsynaptic potential. Since ionic currents depend on the difference in the equilibrium potential and the potential of the membrane, then with a reduced resting potential of the membrane, the Na + ion current is weakening, and the ion current is growing, which leads to a decrease in the amplitude of the exciting postsynaptic potential. Toki Na + and K +, involved in the emergence of an exciting postsynaptic
Fig. 1.27.The diagram of the receptor structure.
BUT- Metabotropic. B.- ionotropic: 1 - neuromodulators or medicines; 2 - receptors with different binding sites (heteroceptor); 3 - neuromodulation; 4 - secondary messenger; 5 - autorceptor; 6 - feedback; 7 - embedding of the membrane of vesicles; 8 - neuromodulators; 9 - transmitter; 10 - neuromodulation; 11-transmitter catalyzes the reactions of G-proteins; 12 - Transmitter opens the ion channel
which potential behave differently than when generating the capacity of the action, since other ion channels with other properties take part in the mechanism of postsynaptic depolarization. If potential-governed ion channels are activated when generating the potential of the action, and when depolarization is increasing, other channels are opened, as a result of which the depolarization process enhances itself, the conductivity of transmitter-controlled (ligandal) channels depends only on the number of transmitter molecules that have contacted receptors, i.e. on the number of open ion channels. The amplitude of the exciting postsynaptic potential is from 100 μV to 10 mV, the potential duration is in the range from 4 to 100 ms, depending on the type of synapse.
The exciting postsynaptic potential, which formed in the synapse zone, is passively distributed throughout the postsynaptic cell membrane. With the simultaneous excitation of a large number of synapses, the phenomenon of the summission of postsynaptic potential occurs, manifested by a sharp increase in its amplitude, as a result of which the membrane of the entire postsynaptic cell can be depolarized. If the depolarization value reaches the threshold value (more than 10 mV), then the generation of the action potential begins, which is carried out on the axon of the postsynaptic neuron. From the beginning of the exciting postsynaptic potential before the formation of the action potential passes about 0.3 ms, i.e. In case of massive release of the neurotransmitter, the postsynaptic potential may appear after 0.5-0.6 ms from the moment of coming to the presynaptic area of \u200b\u200bthe action potential (the so-called synaptic delay).
The postsynaptic receptor protein may have high affinity of other connections. Depending on how (with respect to the neurotransmitter), the effect leads to their receptor binding, the agonists (unidirectional effect with the neurotransmitter) and antagonists (the action of which prevents the effects of the neurotransmitter).
There are receptor proteins that are not ion channels. When binding to them, the neurotransmitter molecules arises a cascade of chemical reactions, as a result of which neighboring ion channels open with secondary messengers - metabotropic receptors.An important role in their functioning is played by G-protein. The synaptic transmission in which the metabotropic reception is used is very slow, the impulse transmission time is about 100 ms. To synapses
this type includes postganglyonic receptors, receptors of the parasympathetic nervous system, auto beceptors. An example is the cholinergic synaps of a muscarinic type, in which the zone of the binding of the neurotransmitter and the ion channel are not localized in the transmembrane protein itself, metabotropic receptors are associated directly with G-protein. When binding a transmitter with a G-protein receptor having three subunits, a complex forms with a receptor. The GDF associated with the G-protein is replaced by the GTF, while the G-protein is activated and acquires the ability to open a potassium ion channel, i.e. hyperpolarize postsynaptic membrane (see Fig. 1.27).
Secondary messengers can open or close ion channels. Thus, ion channels can be opened using CAMF / IP 3 or phosphorylation of protein kinase C. This process also passes with the G-protein, which activates phospholipase C, which leads to the formation of inositatriphosphate (IP 3). Additionally, the formation of diacylglycerol (DAG) and protein kinases with (PKS) increase (Fig. 1.28).
Each nerve cell has many synaptic endings on its surface, some of which are exciting, others -
Fig. 1.28.The role of secondary messengers of inositatriphosphate (IP 3) (BUT)and diacylglycerol (DAG) (B)in the work of the metabotropic receptor. When binding a mediator with a receptor (P), a change in the conformation of the G-protein is changed, followed by the activation of phospholipase C (Fls). Activated Fls splits phosphatidylindalitrophosphate (PIP 2) per DAG and IP 3. Dag remains in the inner layer of the cell membrane, and IP 3 diffuses to cytosol as a secondary intermediary. Dag is built into the inner layer of the membrane, where it interacts with proteinkinase with (PKS) in the presence of phosphatidylserine (FS)
molds. If the adjacent excitation and brake synapses are activated in parallel, the emerging currents are superimposed on each other, as a result there is a postsynaptic potential with an amplitude of less than separately its exciting and braking components. At the same time, the hyperpolarization of the membrane is essential due to increasing its conductivity for ions to + and C1.
Thus, the exciting postsynaptic potential is generated by increasing the permeability for Na + ions and the incoming current of Na + ions, A brake postsynaptic potential is generated due to the output current of K + ions or incoming current ions C1 -. The decrease in conductivity for ions to + should depolarize the cell membrane. Synaps, in which depolarization is caused by a decrease in conductivity for ions K +, is localized in the ganglia of the vegetative (autonomous) nervous system
Synapic transfer must be quickly completed so that the synapse is ready for a new transfer, otherwise the answer would not have occurred under the influence of new signals, would have been observed depolarization unit.An important mechanism of regulation is the rapid decrease in the sensitivity of the postsynaptic receptor (desensitization), which occurs with still persisting neurotransmitter molecules. Despite the continuous binding of the neurotransmitter with the receptor, the conformation of the channel-forming protein changes, the ion channel becomes impermeable for ions and the synaptic current stops. In many synapses, the receptor desensitization can be long (up to several minutes) until the reconfiguration and reactivation of the channel occur.
In other ways of termination of the transmitter, allowing to avoid long-term receptor desessitization, are the rapid chemical splitting of the transmitter to inactive components or its removal from the synaptic slit by highly selective reverse capture of the presynaptic end. The nature of the inactivating mechanism depends on the type of synapse. Thus, acetylcholine is very quickly hydrolyzed by acetylcholineserase for acetate and choline. In the central nervous system, exciting glutamhergic synapses are tightly covered with astrocyte processes, which actively capture the neurotransmitter from the synaptic slit and metabolize it.
1.7. Neurotransmitters and neuromodulators
Neurotransmitters transmit a signal in synapses between neurons or between neurons and actuating agencies (muscle, glandular cells). Neuromodulators are presopentically affect the amount of the neurotransmitter released or its reverse capture of neuron. In addition, neuromodulators are postsynaptically regulate the sensitivity of the receptors. Thus, neuromodulators are able to adjust the level of excitability in synapses and change the effect of neurotransmitters. Neurotransmitters and neuromodulators together form a group of neuroactive substances.
Many neurons are an object of exposure to several neuroactive substances, but only one transmitter is released during stimulation. The same neurotransmitter, depending on the type of postsynaptic receptor, can give an exciting or braking effect. Some neurotransmitters (for example, dopamine) can function both as neuromodulators. In the neurofunctional system, several neuroactive substances are usually involved, while one neuroactive substance is able to influence several neurofunctional systems.
Catecholamiergic neurons
Catecholamiergic neurons contain such neurotransmitters such as dopamine, norepinephrine or adrenaline, which are synthesized from tyrosine amino acids in pericaria. In the brain of an adult, dopaminergic, noradreen and adrenergic neurons on localization correspond to melanin-containing neurons. Noradrenergic and dopaminergic cells are denoted by numbers from A1 to A15, and adrenergic - from C1 to C3, the ordinal numbers are assigned in an increasing order, respectively, the location in the brain barrel from the lower departments to the top.
Dopaminergic neuronsDopamincing cells (A8-A15) are located on average, intermediate and finite brain (Fig. 1.29). The largest group of dopaminergic cells is a compact part of the Black Substance (A9). Their axons form an upward way passing through the lateral part of the hypothalamus and the inner capsule, nigrotrian bundles of
Fig. 1.29.Localization of dopaminergic neurons and their paths in the brain of rats.
1 - cerebellum; 2 - cerebral bark; 3 - striped body; 4 - adjacent kernel; 5 - frontal bark; 6 - olfactory bulb; 7 - olfactory hill; 8 - tail core; 9 - almond-like core; 10 - median elevation; 11 - Nigrostric beam. The main path (nigrostricular beam) begins in black substance (A8, A9) and goes forward to the striped body
cOP reaches a taper kernel and shell. Together with the dopaminergic neurons of the reticular substance (A8), they form a nigrotrorying system.
The main path (nigrostricular beam) begins in black substance (A8, A9) and goes forward to the striped body.
The mesolimbic group of dopaminergic neurons (A10) extends from messephalotic departments to the limbic system. A group A10 forms a ventral vertex in inter-component nuclei in a medium brain coating. Axons are sent to the inner nuclei of the ultimate furrow, partitions, olfactory tubercles, adjacent to the kernel (n. accumbens),walked overwhelming.
The third dopaminergic system (A12), called tuboinfundibular, is located in the intermediate brain, is located in a gray bug and stretches to a funnel. This system is associated with neuroendocrine functions. Other diancephal cells of cells (A11, A13 and A14) and their target cells are also located in the hypothalamus. The small group A15 is dispersed in an olfactory bulb and is the only dopaminergic group of neurons in the final brain.
All dopamine receptors act through the system of secondary messengers. Their postsynaptic action can be exciting or brake. Dopamine quickly captures back to the presynaptic end, which is metabolized by monoaminoxidase (MAO) and Catechol-O-methylTransferase (CT).
Noradrenergic neuronsNoradrenergic nerve cells are only in a narrow front of the tires of the oblong brain and the bridge (Fig. 1.30). In-
Fig. 1.30.Localization of noradreengic neurons and their paths in the head brain of rats (parasagittal slice).
1 - cerebellum; 2 - dorsal beam; 3 - ventral beam; 4 - hippocampia; 5 - cerebral cortex; 6 - olfactory bulb; 7 - partition; 8 - medial front-winged beam; 9 - terminal strip; 10 - hypothalamus.
The main path begins in the blue spot (A6) and goes forward by several beams, giving branches to various brain departments. Also, the noradrenergic nuclei is located in the ventral part of the brain barrel (A1, A2, A5 and A7). Most of their fibers are walking together with the fibers of the blue spots of neurons, but the part is projected in the dorsal direction.
loans coming from these neurons rise to the middle brain or descend to the spinal cord. In addition, the noradreengic cells have a cerebellum connection. Noradrenergic fibers branched extensive than dopaminergic. It is believed that they play a role in the regulation of cerebral blood flow.
The largest group of noradreengic cells (A6) is located in the blue spots. Locus Cereleus)and includes almost half of all noradreengic cells (Fig. 1.31). The kernel is located at the top of the bridge at the bottom of the IV ventricle and extends upwards up to the lower hills of Quadrahmia. The axons of the blue spots cells are repeatedly branched, their adrenergic endings can be found in many CNS departments. They provide a modulating effect on the processes of ripening and training, processing information in the brain, setting sleep and endogenous inhibition of pain.
The rear noradreengic bundle originates from the group A6 and connects in the middle brain with the rear seam nuclei, the upper and lower buccorkas; In the intermediate brain - with the front cores of the Talamus, media and lateral crankshaft; In the final brain - with a almond-shaped body, a hippocampus, neocortex, waist-up.
Additional fibers from the A6 group cells go to the cerebellum through its upper leg (see Fig. 1.31). Downward fibers from the blue spot together with the fibers of the neighboring group of A7 cells go to the rear core of the wandering nerve, lower olive and the spinal cord. Front-hand
Fig. 1.31.The diagram of conducting noradrenergic pathways from the blue kernel (spots) located in the gray matter of the bridge.
1 - fibers of the conductive path; 2 - hippocampus; 3 - Talamus; 4 - hypothalamus and almond-shaped kernel; 5 - cerebellum; 6 - spinal cord; 7 - Blue Spot
howling downward bundle from the blue spot gives fibers to the front and rear horns of the spinal cord.
Neurons of groups A1 and A2 are located in the oblong brain. Together with the group of cells of the bridge (A5 and A7), they form the front ascending noradnergic paths. In the middle brain, they are projected onto a gray-win-conductive core and a reticular formation, in the intermediate brain - on the entire hypothalamus, in the final brain - to the olfactory bulb. In addition, from these cell groups (A1, A2, A5, A7), bobbospinal fibers also go to the spinal cord.
In the PNS Noradrenalin (and to a lesser degree of adrenaline) is an important neurotransmitter of the sympathetic postganglionary endings of the vegetative nervous system.
Adrenergic neurons
Adrenalinesint-sensitive neurons are only in the oblong brain, in a narrow front-flying area. The largest group of C1 cells lies behind the rear olive core, the average group of C2 cells is next to the core of a single path, the C3 cell group is directly under the sloping gray substance. The efferent paths from C1-C3 go to the rear core of the wandering nerve, the kernel of a single path, a blue spot, a sodon-conductive gray substance of the bridge and mid-brain, hypothalamus.
There are 4 main types of catecholarmiergic receptors that differ in the reaction to the action of agonists or antagonists and in postsynaptic effects. The receptors α1 are controlled by calcium channels using the secondary messenger of inositol phosphate-3 and when activated, an intracellular concentration of ions increases
CA 2+. The stimulation of β2 receptors leads to a decrease in the concentration of the secondary Messenger of the CAMF, which is accompanied by various effects. Receptors in via a secondary messenger CAMF increase the conductivity of membranes for ions to + generating braking postsynaptic potential.
Serotonergic neurons
Serotonin (5-hydroxytriptamin) is formed from tryptophan amino acids. Most serotonergic neurons are localized in the medial sections of the brain stem, forming the so-called seam kernels (Fig. 1.32). B1 and B2 groups are located in the oblong brain, B3 - in the border zone between the oblong brain and the bridge, B5 - in the bridge, B7 - in the middle brain. Neurons seam B6 and B8 are in the top of the bridge and middle brain. In the nuclei of the seam, nerve cells containing other neurotransmitters are also located, such as dopamine, norepinerenaline, gamc, enkephalin and substance R. For this reason, the seam kernel is also called multi-edged centers.
Projections of serotonergic neurons correspond to the move of norerangenergic fibers. The bulk of the fibers is sent to the structures of the limbic system, the reticular formation and the spinal cord. There is a bond with a blue spot - the main concentration of the norerangenergic neurons.
A large front-up road rises from the B6, B7 and B7 group cells. It goes a quivering through the tire of the middle brain and laterally through the hypothalamus, then gives the branches towards the severity and the waist overhang. Through this path of the group B6, B7 and B8 are associated with a middle brain with inter-stalk nuclei and a black substance, in the intermediate brain - with the nuclei of a leash, a thalamus and a hypothalamus, in the final brain - with the cores of the partition and an olfactory bulb.
There are numerous projections of serotonergic neurons on a hypothalamus, a waist ulus and an olfactory bark, as well as connections with striatum and frontal bark. The shorter rear upstream path connects the cells of the groups B3, B5 and B7 by means of the rear longitudinal beam with the sodium gray substance and the rear hypothalamic area. In addition, there are serotonergic projections on the cerebellum (from B6 and B7) and the spinal cord (from B1 to B3), as well as numerous fibers connecting with the reticular formation.
Serotonin release occurs in the usual way. The postsynaptic membrane contains receptors, which using secondary messengers open channels for ions to + and Ca 2+. Selects 7 grades of receptors to serotonin: 5-NT 1 - 5-HT 7, differing in the action of agonists and antagonists. 5-HT 1, 5-HT 2 and 5-HT 4 receptors are located in the brain, 5-NT 3 receptors - in PNS. Serotonin action ends with the help of a neurotransmitter reverse capture mechanism with a presynaptic end. Serotonin, who did not arrive in vesicles, is deamined by Mao. There is an inhibitory effect of descending serotonergic fibers on the first sympathetic neurons of the spinal cord. It is assumed that thus neurons of the seam of the oblong brain control the conduct of pain impulses in the anterolateral system. Serotonin deficiency is associated with the emergence of depression.
Fig. 1.32.Localization of serotonergic neurons and their paths in the head brain of rats (parasagittal slice).
1 - olfactory bulb; 2 - belt; 3 - corn body; 4 - brain cortex; 5 - medial longitudinal beam; 6 - cerebellum; 7 - medial front-floor beam; 8 - brain strip; 9 - terminal strip; 10 - arch; 11 - taper core; 12 - external capsule. Serotonergic neurons are grouped into nine kernels located in the brain barrel. Kernels B6-B9 are projected by the kleon to the intermediate and final brain, while the caudal kernels are projected into the oblong and spinal cord
Histaminergic neurons
Histaminergic nervous cells are located at the bottom of the hypothalamus close to the funnel. Histamine is metabolized by the enzyme histidine decarboxylase from histidine amino acid. Long and short bundles of the fibers of histaminergic nerve cells at the bottom of the hypothalamus go to the brain barrel in the rear and perivativericular zone. Histaminergic fibers reach a round-wire gray substance, the rear core of the seam, the medial vestibular nucleus, the nucleus of a single path, the rear nucleus of the vagus nerve, the kernel
facial nerve, front and rear cochlear nuclei, lateral loop and lower buccorkas quirky. In addition, the fibers are sent to the intermediate of the brain - the rear, lateral and front departments of the hypothalamus, the deputy bodies, the visual bug, the perivativericular nuclei, the lateral crankshaft and to the final brain - the diagonal winding of Brock, n. Accumbness,the almond-shaped body and the core of the big brain.
Holieregic neurons
Alpha (α) - and gamma (γ) -motoneons of a oculomotory, block-like, triple, discharge, facial, language, wandering, added and sub-speaking nerves and spinal nerves - cholinergic (Fig. 1.33). Acetylcholine affects the reduction of skeletal muscles. Pregganionic neurons of the vegetative nervous system are cholinergic, they stimulate the postganglyonar neurons of the vegetative nervous system. Other cholinergic nerve cells obtained an alphanumeric designation in the direction from top to bottom (in reverse order compared to catecholamic and serotonergic neurons). Cholinergic neurons CH1 form about 10% of the cells of the median nuclei of the partition, the neurons CH2 are 70% of the cells of the vertical limb of the diagonal stroke of the brocade, the neurons CH3 are 1% of the cells of the horizontal limb of the diagonal stroke of the broc. All three groups of neurons are projected down on the medial kernels of the leash and interchangeable kernels. CH1 neurons are connected by ascending fibers through a hippocampal arch. The CH3 cell group is synaptically associated with the nerve cells of the olfactory bulb.
In the human brain, the CH4 cell group is relatively extensive and corresponds to the basal kernel of meerter, in which 90% of all cells are cholinergic. These kernels receive afferent impulses from subcortical diancefral-teletepheal departments and form a limbico-paralyambic bark of the brain. The front cells of the basal kernel are projected onto the front and parietal neocortex, and the rear cells are on the occipital and temporal neocortex. Thus, the basal core is a transmitting link between limbico-paralyambic departments and neocortex. Two small groups of cholinergic cells (CH5 and CH6) are located in the bridge and are considered as part of the ascending reticular system.
A small group of cellular core cells, partially consisting of cholinergic cells, is located at the edge of the trapezoidal body in the lower sections of the bridge. Its efferent fibers go to the receptor cells of the hearing system. This cholinergic system affects the transmission of sound signals.
Aminacidergic neurons
Neurotransmitter properties are proved for four amino acids: exciting for glutamic (glutamate), asparaginic (aspartate) acids, brakes - for G-amino-oil acid and glycine. The neurotransmitter properties of cysteine \u200b\u200b(exciting) are assumed; Taurine, serine and p-alanine (brake).
Fig. 1.33.Localization of cholinergic neurons and their paths in the brain in rats (parasagittal slice). 1 - almond-like core; 2 - front olfactory core; 3 - arcuate kernel; 4 - Meertain Basal core; 5 - cerebral cortex; 6 - tape tape shell; 7 - diagonal brother of brother; 8 - a bent bundle (Meertain beam); 9 - hippocampus; 10 - interchangeable kernel; 11 - lateral and dorsal tire core; 12 - medial core of the leash; 13 - olfactory bulb; 14 - olfactory hill; 15 - reticular formation; 16 - brain strip; 17 - Talamus; 18 - reticular tire formation
Glutamanthergic and asparthergic neuronsStructurally similar amino acids glutamate and aspartate (Fig. 1.34) electrophysiologically classified as exciting neurotransmitters. Nervous cells containing glutamate and / or aspartate as neurotransmitters are available in the hearing system (first-order neurons), in the olfactory system (combine an olfactory bulb with a large brain cortex), in a limbic system, in neocortex (pyramid cells). Glutamate is also detected in the neurons of conductive paths coming from pyramid cells: corticocent, corticotlamic, corticothactal, curtic and corticospinal paths.
An important role in the functioning of the glutamate system is played by astrocytes that are not passive elements of the nervous system, and the energy substrates involved in providing neurons in response to an increase in synaptic activity. Astrocitary process
Fig. 1.34.Synthesis of glutamic and aspartic acids.
By glycolysis, glucose transformation into pyruvate, which in the presence of acetyl-koa enters into the Krebs cycle. Further, by transamination, oxaloacetate and α-ketoglutate are converted into aspartate and glutamate, respectively (reactions are presented at the bottom of the figure)
ki are located around synaptic contacts, which allows them to capture an increase in the synaptic concentration of neurotransmitters (Fig. 1.35). The transfer of glutamate from the synaptic slit is mediated by specific transport systems, two of which are glialospecific ( GLT-1and Glast-carriers). Third transport system (EAAS-1),located exclusively in neurons, not involved in the transfer of glutamate released from synaps. The glutamate transition to astrocytes occurs according to the electrochemical gradient of Na + ions.
Under normal conditions, the relative constancy of the extracellular concentrations of glutamate and aspartate is maintained. Their increase includes compensatory mechanisms: seizure of neurons and astrocytes of excess from the intercellular space, the presynaptic braking of neurotransmitter emissions, metabolic utilization and
Fig. 1.35.The structure of glutamanthergic synapse.
Glutamate is released from synaptic vesicles into the synaptic gap. The figure shows two reverse capture mechanisms: 1 - back to the presynaptic ending; 2 - in the adjacent glial cell; 3 - clay cell; 4 - axon; 5 - glutamine; 6 - glutamine synthetase; 7 - ATP + NH 4 +; 8 - glutaminase; 9 - glutamate + NH 4 +; 10 - glutamate; 11 - postsynaptic membrane. In glutamy glutaminsintase cells, glutamate turns into glutamine, which next goes into the presynaptic end. In the presynaptic end, glutamine turns back to glutamate with glutamine enzyme. Free glutamate is also synthesized in the Krebs cycle reactions in mitochondria. Free glutamate is assembled in synaptic vesicles before the appearance of the following potential of action. The right part of the figure shows the reaction of the transformation of glutamate and glutamine, mediated by glutamine substate and glutamine
other in violation of their elimination from the synaptic slit The absolute concentration and time of the depression of glutamate and aspartate in the synaptic slit exceeds the permissible limits, and the neuron membrane depolarization process becomes irreversible.
The mammalian CNS exists families of ionotropic and metabotropic glutamate receptors. Ionotropic receptors regulate the permeability of ion channels and are classified depending on the sensitivity to the action of N-methyl-D-aspartate (NMDA),α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMRA),cainic acid (K) and L-2-amino-4-phosphonasyl acid (L-AP4)- The most selective ligands of this type of receptors. The names of these compounds and were assigned to the appropriate types of receptors: NMDA, AMRA, Kand L-AP4.
The most studied NMDA-type receptors (Fig. 1.36). Postsynaptic receptor NMDAit is a complex supramolecular formation, including several sites (sections) of the regulation: the site of the specific binding of the mediator (L-glutamic acid), the site of the specific binding of the coagonist (glycine) and alto-cell modulatory sites, located both on the membrane (polyamine) and in the ion canal Coming with a receptor (binding sites of bivalent cations and a "fencyclic" site - a plot of binding non-competitive antagonists).
Ionotropic receptors play a key role in the implementation of exciting neuroration in the CNS, the implementation of neuroplasticity, the formation of new synapses (synapotogenesis), in increasing the efficiency of the functioning of existing synapses. With these processes, memory mechanisms, training (purchase of new skills), compensation of functions disturbed due to organic brain lesions are largely connected.
Exciting aminoacidergic neurotransmitters (glutamate and aspartate) under certain conditions is characteristic of cytotoxicity. With their interaction with over-excited postsynaptic receptors, dendroscomatic lesions are developing without changes in the conductive part of the nervous cell. Conditions that create such over-use are characterized by increased excretion and / or reduced re-capture of the carrier. Overexcitation of glutamate precisely receptors NMDAleads to the discovery of aging
nista-dependent calcium channels and a powerful influx of Ca 2+ in neurons with a sudden increase in its concentration to the threshold. Caused by excessive aminoacidergic neurotransmitters "Exightotoxic death of neurons"it is a universal mechanism for damage to the nervous tissue. It underlies the necrotic death of neurons in various diseases of the brain, both sharp (ischemic stroke) and chronic (ne-
Fig. 1.36.Glutamate nmda-re-
riesgeneration). The extracellular levels of aspartate and glutamate, and, consequently, the severity of exaitotoxicity affect the temperature and pH of the brain, extracellular concentrations of monovalent ions C1 - and Na +. Metabolic acidosis inhibits glutamate transport systems from the synaptic gap.
There are data on the neurotoxic properties of glutamate associated with the activation of amra and K-receptors, leading to a change in the permeability of the postsynaptic membrane for monovalent cations K + and Na +, enhance the incoming current of the Na + ions and short-term depolarization of the postsynaptic membrane, which, in turn, causes amplification SA 2+ tributary in a cell through agonist-dependent (receptors Nmda)and potential-dependent channels. The Na + ion stream is accompanied by an entrance to water cells, which causes the swelling of apical dendrites and lysis of neurons (osmolatic damage to neurons).
Metabotropic glutamate receptors associated with G-protein plays an important role in the regulation of intracellular calcium current caused by the activation of NMDA receptors, and modulatory functions are performed, thereby causing changes in cell activity. These receptors do not affect the functioning of ion channels, but stimulate the formation of intracellular intermediaries of diacylglycerol and nositatrimphosphate, participating in the further processes of the ischemic cascade.
Hamkergic neurons
Some neurons as a neurotransmitter contain M-aminobacing acid (GABA), which is formed from glutamic acid under the action of glutamatdecarboxylase (Fig. 1.37). In the large brain core, gamkergic neurons are located in olfactory and limbic areas (basket neurons of the hippocampus). GABA also contain neurons of efferent extrapyramidal striatonigital, palloidonigraral and subtalamopalladian paths, cerebellum purking cells, cerebellum cere neurons (Golges, star and basket), insert brake neurons of the spinal cord.
GABA is the most important brake neurotransmitter of the CNS. The main physiological role of GABC is the creation of a steady equilibrium between exciting and braking systems, modulation and regulation of the activity of the main excitatory neurotransmitter of glutamate. GABA limits the distribution of an exciting stimulus as presopriate - through GAB-B-receptors, function-
Fig. 1.37.The reaction of the transformation of glutamate in the gamke.
For the activity of decarboxylase of glutamic acid (DGK) requires a coenidation of pyridoxalphosphate
Fig. 1.38.GAMK receptor.
1 - benzodiazepine-binding site;
2 - GABA-binding site; 3 - ion channel for cl -; 4 - Barbituat-binding site
but associated with potential-dependent calcium channels of presopreptic membranes and postsynaptically - through the GAMA receptors (GABBBITRATBENZODIAZEPIN-receptor complex), functionally related to potential-dependent chlorine channels. Activation of postsynaptic gamke-A receptors leads to hyperpolarization of cell membranes and braking of an exciting pulse caused by depolarization.
The density of gamke-a-receptors is maximum in the temporal and frontal crust, hippocampus, almond and hypothalamic nuclei, a black substance, a sodium gray matter, cerebellum kernels. Several to a lesser extent receptors are presented in the taper core, shell, thalamus, occipital core, epiphysis. All three subunits of the GAMK-A receptor (α, β and γ) are associated with GAB, although the most high binding affinity with a b-subunit (Fig. 1.38). Barbiturates interact with A- and P-subunits; Benzodiazepines - only with a 7-subnce. The affinity of the binding of each of the ligands increases, if other ligands interact with the receptor in parallel with the receptor.
Glycinergic neuronsGlycine is a brake neurotransmitter in almost all CNS departments. The greatest density of glycine receptors was found in the structures of the trunk, the crust of large hemispheres, striatum, hypothalamus kernels, conductor from the frontal cortex to the hypothalamus,
snack, spinal cord. Glycine exhibits inhibitory properties by interaction not only with its own strikhinno-sensitive glycine receptors, but also with GABA receptors.
In small concentrations, glycine is necessary for the normal functioning of glutamate receptors NMDA.Glycine is a co-agonist of receptors NMDA,since their activation is possible only under the condition of binding glycine with specific (insensitive to strikhnin) by glycine sites. Glicin potentiary action for receptors NMDAit is manifested in concentrations below 0.1 μmol, and at a concentration of from 10 to 100 μmol, the glycine site is completely saturated. High concentrations of glycine (10-100 mmol) do not activate NMDA-induced depolarization in vivo.and, therefore, do not increase exaitotoxicity.
Peptidergic neurons
Neurotransmitter and / or neuromodulatory function of many peptides is still studied. Peptidergic neurons include:
Hypothalamoneryrhypofizar nervous cells with peptides
Sitocin and vasopressin as neurotransmitters; hypophizate cells with peptides somatostatin, cortic
quiberine, Tyrolyiberin, Luliberin;
Neurons with peptides of the vegetative nervous system of the gastrointestinal tract, such as substance p, vasoactive intestinal polypeptide (wines) and cholecystokinin;
Neurons whose peptides are formed from pro-opiomelanocortin (corticotropin and β-endorphine),
Encofalinergic nerve cells.
Substance-P - containing neuronsSubstance P - peptide of 11 amino acids, which has a slowly starting and long continued exciting effect. Substance R contain:
About 1/5 of the spinal ganglia and trigeminal (Hasserov) of Ganglia, whose axons have a subtle myelin shell or are not immaculated;
Cells of olfactory bulbs;
Neurons of the occasional gray matter;
Neurons of the path coming from the middle brain to the intercoms of the nuclei;
Neurons of efferent nigrostrix paths;
Small nerve cells located in a large brain core, mainly in V and Vi layers.
VIP-containing neuronsVasoactive intestinal polypeptide (VIP) consists of 28 amino acids. In the nervous system, the VIP is an exciting neurotransmitter and / or neuromodulator. The greatest concentration of VIP is found in neocortex, mainly in bipolar cells. In the brain barrel, VIP-containing nerve cells are located in the single path core and are associated with the limbic system. In the suprahiasmal core there are VIP-containing neurons associated with the nuclei of the hypothalamus. The gastrointestinal tract has a vasodilating effect and stimulates the glycogen transition to glucose.
β-endorphin-containing neuronsβ -endorphine - peptide of 31 amino acids functioning as a brake brake neuromodulator. Endorphinegic cells are located in the mediobasal hypothalamus and in the lower sections of the nucleus of a single path. The ascending endorphinegic pathways from the hypothalamus are sent to the preoptic field, the cores of the partition and the almond-shaped body, and the descending paths go to the occasional-conductive gray substance, the blue kernel and the reticular formation. Endorphinery neurons are involved in the central regulation of the analgesia, they stimulate the release of growth hormone, prolactin and vasopressin.
Enkephalinergic neurons
Enkephalin - peptide of 5 amino acids, functioning as an endogenous ligand of opiate receptors. Enkefalinergic neurons are located in the surface layer of the rear horns of the spinal cord and the kernel of the spinal path of the trigeminal nerve, the periodal core (the auditory system), olfactory bulbs, in the seam kernels, in the gray colonium substance. Enkephalin-containing neurons are also in neocortex and Allooktex.
Encofalinergic neurons presopriately inhibit the release of substance p from the synaptic endings of afferents conductive pain impulses (Fig. 1.39). Analgesia can be achieved by electrostimulation or opiate micro enterprises to this area. Encofalinergic neurons affect the hypothalamic-pituitary regulation of the synthesis and isolation of oxytocin, vasopressin, some liberins and statins.
Nitrogen oxide
Nitrogen oxide (NO) is a polyfunctional physiological regulator with a neurotransmitter properties, which, unlike traditional neurotransmitters, is not reserved in the synaptic vesicles of nerve endings and is released into the synaptic slit by free diffusion, and not according to the exocitation mechanism. The NO molecule is synthesized in response to the physiological need of WA-synthase enzyme (WAS) from L-arginine amino acid. The ability to give the biological effect is mainly small in the size of its molecule, its high reactivity and diffusion ability in tissues, including nervous. This served as the basis to name the NO retrograde messenger.
Mix three forms WAV. Two of them are constitutive: neuronal (NCNOS) and endothelial (ECWAS), the third - inducible (WAV) detected in the cells of the Glia.
Calcium-calmodulin-dependence of the neuronal Isoform WAV determines the amplification of the NO synthesis when increasing the level of intracellular calcium. In this regard, any processes leading to calcium accumulation in the cell (energy deficiency, changes in active ion transport,
Fig. 1.39.The mechanism of enkefalinergic regulation of pain sensitivity at the level of the journalist substance.
1 - interneurone; 2 - Enkephalin; 3 - enkefalin receptors; 4 - rear horns of the spinal cord; 5 - Receptors Substance P; 6 - Substance P; 7 - Sensitive Neuror of the Spinal Ganglia. In the synapse between the peripheral sensitive neuron and neuron of the spinnotelamic ganglium, the main mediator is P. Enkefalinergic interneamon reacts to pain sensitivity, having a premugustic inhibitory effect on the release of substance P
glutamatic exaitotoxicity, oxidant stress, inflammation) are accompanied by an increase in the level of NO.
It is shown that NO has a modulating effect on synaptic transmission, on the functional state of glutamate NMDA receptors. Activating the soluble heme-containing guanillatcyclasis, NO is involved in the regulation of intracellular concentration of Ca 2+ ions, pH inside the nerve cells.
1.8. Axion transport
Anxual transport is played in internecronal connections. Membrane and cytoplasmatic community components that are formed in the biosynthesting device of the Soma and the proximal portion of dendrites should be distributed across the axon (their admission to the premipatical structures of synapses is especially important) to fill the loss of elements that have been released or inactivation.
However, many axons are too long that materials can effectively move from the Soma to synaptic endings by simply diffusion. This task is performed by a special mechanism - axonal transport. There are several types of it. Orgella and mitochondria surrounded by membranes are transported from a relatively high speed through rapid axonal transport. Substances dissolved in cytoplasm (for example, proteins) are moved by slow axonal transport. In mammals, rapid axonal transport has a speed of 400 mm / day, and slow - about 1 mm / day. Synaptic bubbles can act with the help of rapid axonal transport from the Soma Motoneron of the spinal cord of the person to the muscles of the foot after 2.5 days. Compare: Delivery to the same distance of many soluble proteins takes about 3 years.
For axonal transport, the cost of metabolic energy and the presence of intracellular calcium are required. The elements of the cytoskeleton (more precisely, the microtubule) create a system of guide of heavy, along which the organelles surrounded by membranes. These organelles are attached to microtubules in the same way as it occurs between thick and thin fibers of skeletal muscles; Organelle movement along the microtubule is launched by ions Ca 2+.
Axion transport is carried out in two directions. Transportation from the soma to axonal terminals, called anterograde axon transport, replenishes the stock of synaptic bubbles and enzymes responsible for the synthesis of the neurotransmitter in the presynaptic endings. Transport in the opposite direction is a retrograde axon transport, returns devastated synaptic bubbles in a matter where these membrane structures are degraded by lysosomes. The substances coming from synapses are necessary to maintain the normal metabolism of the bodies of nerve cells and, in addition, carry information about the state of their end machines. The violation of retrograde axonal transport leads to changes in the normal operation of nerve cells, and in severe cases - to retrograde degeneration of neurons.
The axonal transport system is the main mechanism that determines the renewal and supply of mediators and modulators in the presynaptic endings, and also underlies the formation of new processes, axons and dendrites. According to the ideas about the plasticity of the brain as a whole, two interrelated processes are constantly in the brain of an adult: the formation of new processes and synapses, as well as the destruction and disappearance of some part of the previously existed internersion contacts. Axonial transport mechanisms associated with them The processes of synaptogenesis and the growth of the subtlest axon branchings underlie learning, adaptation, compensation for disturbed functions. Axonial disorder leads to the destruction of synaptic endings and changing the functioning of certain brain systems.
Drug and biologically active substances can affect the metabolism of neurons, determining their axonial transport, stimulating it and increasing the possibility of compensatory regenerative processes. Strengthening axonal transport, the growth of the finest branches of axons and synaptogenesis play a positive role in the normal operation of the brain. In pathology, these phenomena underlie the reparative, compensatory restoration processes.
Through axonal transport in peripheral nerves, some viruses and toxins are distributed. So, chickenpox virus VARICELLA ZOSTER VIRUS)penetrates the cells of the cerebrospinal (spinal) ganglia. There, the virus is in inactive form sometimes for many years until the immune status of man changes. Then the virus can be transported by touch axon to the skin, and in dermatomas
painful spinal nerves arise painful rashes (Herpes Zoster).The axle-tax transport is transferred and tetanical toxin. Bacteria Clostridium Tetani.from a contaminated wound by retrograde transport in motorway. If the toxin comes into the extracellular space of the front horns of the spinal cord, it blocks the activity of the synaptic receptors of brake neuromediator amino acids and will cause the tetanic seizures.
1.9. Nervous tissue reactions for damage
Damage to the nervous tissue is accompanied by reactions of neurons and neuroglia. In case of severe damage, the cells die. Since neurons are postmitic cells, they are not replenished.
Mechanisms of death of neurons and cells of Glia
In strongly damaged tissues, necrosis processes are predominant, affecting whole cell fields with passive degeneration of cells, swelling and fragmentation of organelles, the destruction of membranes, cell lysis, the output of intracellular content in the surrounding tissue and the development of an inflammatory response. Necrosis is always due to coarse pathology, its mechanisms do not require energy costs and it is possible to prevent it only by removing the cause of damage.
Apoptosis- Type of programmed cell death. Apoptotic cells, as opposed to necrotic, are arranged by one or small groups, scattered throughout the tissue. They have a smaller size, unchanged membranes crossed by cytoplasm with the preservation of the organelle, the appearance of multiple cytoplasmic membranes associated tops. There is no inflammatory tissue reaction, which is currently served by one of the important distinctive morphological signs of apoptosis from necrosis. And wrinkled cells, and apoptotic tales contain intact cellular organelles and mass of condensed chromatin. The result of the consistent destruction of DNA in apoptar cells becomes the impossibility of their replication (reproduction) and participation in intercellular interactions, since these processes require the synthesis of new proteins. Dying cells are effectively removed from the fabric by phagocytosis. The main differences in the processes of necrosis and apoptosis are summarized in Table. 1.1.
Table 1.1.Signs of differences in necrosis and apoptosis processes
Apoptosis is an integral part of the development processes and homeostasis of mature tissue. Normally, the body uses this genetically programmed mechanism in embryogenesis to destroy the "excess" of cellular material at an early stage of the development of tissues, in particular in neurons who did not establish contacts with target cells and devoid, thus trophic support from these cells. In the adulthood, the intensity of apoptosis in the Mammamy CNS is significantly reduced, although it remains high in other tissues. The elimination of the cells affected by viruses, the development of an immune response is also accompanied by an apoptotic response. Along with apoptosis, other variants of programmed cell death are distinguished.
The morphological markers of apoptosis are apoptotic tales and wrinkled neurons with a holistic membrane. The biochemical marker, which has become practically identical to the concept of "apoptosis", consider DNA fragmentation. This process is activated by ions Ca 2+ and Mg 2+, and inhibited by Zn 2+ ions. DNA splitting occurs as a result of the action of calcium-magnesium-dependent endonuclease. It has been established that endonucleases split the DNA between proteins by histones, released fragments of regular length. DNA is initially divided into large fragments of 50 and 300,000 bases, which are then split into parts of 180 pairs of bases forming the "stairs" during separation by gel electrophoresis. DNA fragmentation does not always correlate with the morphology characteristic of apoptosis and is a conditional marker, non-equivalent morphological criteria. The most perfect to confirm the apoptosis is the biologically-histochemical method, which allows you to fix not only DNA fragmentation, but also an important morphological basis - apoptotic taurus.
The apoptosis program consists of three consecutive stages: making decisions on death or survival; implementation of the extermination mechanism; Elmination of dead cells (degradation of cellular components and their phagocytosis).
Survival or death of cells is largely determined by the expression products of the CW-family genes. Protein products of two of these genes, cED-3.and cED-4.("Murderer's genes") are necessary for the flow of apoptosis. Protein product Gena cED-9.protects cells, preventing apoptosis by preventing the excitation of genes cED-3.and cED-4.The rest of the genes of the family cEDcoding proteins involved in packaging and phagocytosis of dying cells, degradation of DNA dead cell.
Mammal Homologists Milk Gene cED-3.(and its protein products) are genes encoding interleukin-sparing enzymes - caspases (cysteine \u200b\u200baspartyl proteases), which have different substrate and inhibitory specificity. Inactive predecessors of Caspaz - Dolpaspaz are present in all cells. Activation of pumppass in mammals is carried out by an analogue of a CED-4-gene - an exciting factor of apoptotic proteas - 1 (APAF-A),there is a binding place for ATP, which emphasizes the significance of the level of energy support for the choice of the death mechanism. When exciting caspases modify the activity of cell proteins (polymeraz, endonucleases, components of the nuclear membrane), which are responsible for fragmentation of DNA in apoptotic cells. Activated enzymes begin to split DNA with the appearance of trifosphonucleotides in places, causes the destruction of cytoplasma proteins. The cell loses water and decreases, the pH of the cytoplasm decreases. The cell membrane loses its properties, the cell is wrinkled, apoptotic tales are formed. The process of adjusting the cell membranes is based on the activation of siringomylase, which cleaves the cells of cells with the release of the ceramide activating the phospholipase A2. Arachidonic acid accumulation occurs. The phosphatidylserine proteins expressed during apoptosis and vitrenectin are removed on the outer surface of the cell and signal macrophages that performs phagocytosis of apoptotic taurus.
Homologists gene nematodes cED-9,determining the survival rate of cells, in mammals is a family of protoncogen bCL-2.AND bCL-2,and child protein bCL-X-Lpresented in the mammalian brain, where they protect neurons from apoptosis with ischemic effects, removal of growth factors, the effects of neurotoxins in vivo.and in vitro.Analysis of products for expression of BCL-2-genes revealed a whole family of BCL-2-related proteins, which includes antipoptotic (BCL-2and BCL-X-L),so and prohapoptosis (BCL-X-S, BAX, BAD, BAG)proteins. Pros and BAD proteins have a homologous sequence and form heterodimers with bCL-2and bcl-X-L in vitro.For activity, overwhelming death, bCL-2and bCL-X-Lmust form dimers with protein Lah,and dimers with protein BAD strengthen death. This made it possible to conclude that bCL-2and relative molecules are key determinants of cell survival or cell death in the central nervous system. Molecular genetic studies have established that so
called gene family bCL-2,consisting of 16 genes with opposite functions, a person is mapping on chromosome 18. Anti-apoptotic effects give six family genes, like the progenitor of the group bCL-2;other 10 genes support apoptosis.
Pro- and anti-apoptotic effects of activated gene expression products bCL-2implemented through the modulation of the activity of mitochondria. Mitochondria is a key figure of apoptosis. It contains cytochrome C, ATP, Ca 2+ ions and apoptosinducing factor (AIF) are the components necessary to induce apoptosis. The yield of these factors from mitochondria occurs when its membrane interacts with activated proteins of the family bCL-2,which are attached to the outer membrane of mitochondria in places of convergence of the outer and inner membranes - in the region of the so-called permeabilization pore, which is a megakanal diameter of up to 2 nm. When attaching proteins bCL-2the outer membrane of mitochondria megakanal pores expand to 2.4-3 nm. On these channels, cytochrome C, ATP and AIF are coming to cytosol cells from mitochondria. Antiapoptotic family squirrels bCL-2,on the contrary, the megakanals are closed, interrupting the promotion of the apoptotic signal and protecting the cell from apoptosis. In the process of apoptosis, mitochondria does not lose its integrity and is not destroyed. Vastered from Mitochondria cytochrome C forms a complex with a factor arbitrating apoptotic protease (APAF-L), Caspase-9 and ATP. This complex is an apoptosoma, in which the Caspase-9 activation is activated, and then the main "killerny" caspase-3, which leads to the death of the cell. Mitochondrial signaling mechanism is the main way induction of apoptosis.
Another mechanism of induction of apoptosis is the transmission of a pro -opopotic signal when linking a ligand with receptors of a cell death region, which occurs with the help of adapter proteins FADD / MORT1, TRADD. The receptor path of cell death is significantly shorter than mitochondrial: according to the means of adaptor molecules, the Caspase-8 activation occurs, which, in turn, directly activates the "killer" caspases.
Certain proteins, such as p53, P21 (WAF1),can contribute to the development of apoptosis. It is shown that natural p53causes apoptosis in tumor cell lines and in vivo.Transformation p53from natural type in a mutant form leads to the development of cancer in many organs as a result of suppressing apoptosis processes.
Decelection axon
After the axon's cut in the Nervous cell soma, the so-called axon reaction is developing, aimed at restoring the axon by the synthesis of new structural proteins. In soma, the intact neurons of the Nissle Taurus are intensively painted by the main aniline dye, which binds to ribone-leather acid ribonucleic acids. However, during the axon reaction, the tank of the rough endoplasmic reticulum is increased in the amount by filling the protein synthesis products. Chromatolysis occurs - disorganization of ribosomes, as a result of which the staining of the Nissl Taurus basic aniline dye becomes much weaker. The body of the cell swells and is rounded, and the kernel shifts to one side (eccentric position of the kernel). All these morphological changes are the reflection of cytological processes accompanying the enhanced protein synthesis.
A axon's plot distal than the location is dying. For several days, this site and all the synaptic endings of the axon are destroyed. The Micheeline Sheath of Akson also degenerates, its fragments are captured by phagocytes. However, neuroglia cells forming myelin do not die. This sequence of phenomena received the name of Wallerian degeneration.
If the damaged axon provided the only or main synaptic input to the nervous or to the effector cell, then the postsenphetic cell can be subjected to degeneration and die. Well known example - atrophy of the fibers of the skeletal muscle after violating their innervation by motor mechanons.
Axon Regeneration
After the degeneration of the damaged axon, many neurons can grow a new axon. At the end of the proximal segment Axon begins to branch up [Splatte Spruting)- Expanding]. In PNS, newly formed branches grow along the source path of the deceased nerve, unless, of course, this path is available. During the Wallerian degeneration period, Schwann cells of the distal part of the nerve are not only survived, but also proliferate, building up the rows where the deceased nerve passed. The "cones of growth" of the regenerating axon lay their ways between the ranks of Schwann cells and ultimately can achieve their targets, reinvating them. Then axons are reeerinized by Schwann cells. Regeneration rate limited
speed \u200b\u200bspeed of slow axon transport, i.e. Approximately 1 mm / day.
Axon regeneration in the central nervous system has some differences: Oligodendroge's cells cannot outline the path for the growth of the axon's branches, since each oligodendrocyte has many axons in the CPS (in contrast to Schwan cells in PNS, each of which has only one axon in myelin).
It is important to note that chemical signals act differently on regeneration processes in the central nervous system and PNS. An additional obstacle to the regeneration of axons in the central nervous system is the glial scars formed by astrocytes.
Synapic spruiting, providing "reusing" of existing neuronal currents and the formation of new polysinapotic bonds, causes the plasticity of neuronal tissue and forms mechanisms involved in the restoration of disturbed neurological functions.
Trophic factors
An important role in the development of ischemic damage to the brain tissue plays the level of its trophic support.
Neurotrophic properties are inherent in many proteins, including structural proteins (for example, S1OOβ). At the same time, they are maximally implemented by growth factors that represent a heterogeneous group of trophic factors consisting of at least 7 families - neurotrophins, cytokines, fibroblastic growth factors, insulin-dependent growth factors, a family of transforming growth factor 31 (TGF-J3i),epidermal growth factors and others, including growth protein 6 (GAP-6) 4, thrombocyt-dependent growth factor, heparin-knitted neurotrophic factor, erythropoietin, macrophageal colonistimulating factor, etc. (Table 1.2).
Neurotrophins are the most powerful trophic effect on all major processes of neurons - regulatory proteins of nervous tissue, which are synthesized in its cells (neurons and glia). They act locally - at the place of release and especially intensively induce the branching of dendrites and the growth of axons in the direction of target cells.
To date, three neurotrofin, close to each other in structure: a factor of nerve growth (NGF), growth factor isolated from brain (BDNF), and neurotrophin-3 (NT-3).
Table 1.2.Modern classification of neurotrophic factors
In a developing body, they are synthesized by the target cell (for example, muscle spindle), diffuse towards neuron, are associated with receptor molecules on its surface.
Recipient-related growth factors are captured by neurons (i.e., endocytosis is subjected to) and transported retrograde in a matter. There they can act directly on the nucleus, changing the formation of enzymes responsible for the synthesis of neurotransmitters and the growth of axons. There are two forms of receptors to growth factors - low-uphine receptors and high-phthine tyrosine kinase receptors, with which most trophic factors associate.
As a result, Akson reaches the target cells by installing synaptic contact with it. Growth factors maintain the life of neurons, which in their absence cannot exist.
Trophy disriselation is one of the universal components of the pathogenesis of damage to the nervous system. When depriving the trophic support for mature cells, biochemical and functional dedifferentiation of neurons with changes in the properties of innervated tissues is developing. Trophy disriselation affects the state of macromolecules involved in membrane electrogenesis, active ion transport, synaptic transmission (enzymes of the synthesis of mediators, postsynaptic receptors) and effector function (muscular myozic). The ensembles of dedifferentiated central neurons create foci of pathologically reinforced excitation, which launching pathobochemichss cascades, which lead to the death of neurons in necrosis and apoptosis mechanisms. On the contrary, with a sufficient level of trophic support for the regression of the neurological deficit after ischemic damage to the brain, it is often observed even with the remaining morphological defect, which initially caused it, which indicates a high adaptability of the brain function.
It has been established that changes in the deficiency of trophic support are involved in the development of potassium and calcium homeostasis, excess synthesis of nitrogen oxide, which blocks the Tyrrosinkinase enzyme, which is included in the active center of trophic factors, and cytokine imbalances. One of the alleged mechanisms is autoimmune aggression against its own neurotrophins and structural neurospecific proteins that have trophic properties, which becomes possible as a result of a violation of the protective function of the hematorecephalic barrier.