Physiological role of central inhibition. Inhibition (physiology). Volpe psychotherapy method

The manifestation and implementation of a reflex is possible only if the spread of excitation from one nerve center to another is limited. This is achieved by the interaction of excitation with another nervous process, the opposite in effect to the process of inhibition.

Almost until the middle of the 19th century, physiologists studied and knew only one nervous process- excitement.

Phenomena of inhibition in nerve centers, i.e. in the central nervous system were first discovered in 1862 by I.M. Sechenov (“Sechenov’s inhibition”). This discovery played no less a role in physiology than the formulation of the concept of reflex itself, since inhibition is necessarily involved in all nervous acts without exception. I.M. Sechenov discovered the phenomenon of central inhibition during irritation of the diencephalon of warm-blooded animals. In 1880, the German physiologist F. Goltz established the inhibition of spinal reflexes. N.E. Vvedensky, as a result of a series of experiments on parabiosis, revealed the intimate connection between the processes of excitation and inhibition and proved that the nature of these processes is the same.

Inhibition is a local nervous process leading to suppression or prevention of excitation. Inhibition is an active nervous process, the result of which is the limitation or delay of excitation. One of characteristic features inhibitory process - lack of ability to actively spread through nerve structures.

Currently, two types of inhibition are distinguished in the central nervous system: central (primary) inhibition, which is the result of excitation (activation) of special inhibitory neurons, and secondary inhibition, which is carried out without the participation of special inhibitory structures in the very neurons in which excitation occurs.

Central inhibition (primary) is a nervous process that occurs in the central nervous system and leads to the weakening or prevention of excitation. According to modern concepts, central inhibition is associated with the action of inhibitory neurons or synapses that produce inhibitory mediators (glycine, gamma-aminobutyric acid, and a type of electrical changes called inhibitory postsynaptic acid), which cause special potentials (IPSP) on the postsynaptic membrane or depolarization of the presynaptic nerve ending with which it is in contact. another nerve ending of the axon. Therefore, central (primary) postsynaptic inhibition and central (primary) presynaptic inhibition are distinguished.

Postsynaptic inhibition (Latin post behind, after something + Greek sinapsis contact, connection) is a nervous process caused by the action of specific inhibitory mediators (glycine, gamma-aminobutyric acid) secreted by specialized presynaptic nerve endings on the postsynaptic membrane. The mediator released by them changes the properties of the postsynaptic membrane, which suppresses the cell’s ability to generate excitation. In this case, there is a short-term increase in the permeability of the postsynaptic membrane to K+ or CI- ions, causing a decrease in its input electrical resistance and the generation of an inhibitory postsynaptic potential (IPSP).

The occurrence of IPSP in response to afferent stimulation is necessarily associated with the inclusion of an additional link in the inhibitory process - an inhibitory interneuron, the axonal endings of which release an inhibitory transmitter. The specificity of inhibitory postsynaptic effects was first studied in mammalian motor neurons. Subsequently, primary IPSPs were recorded in interneurons of the spinal and medulla oblongata, in neurons of the reticular formation, cerebral cortex, cerebellum and thalamic nuclei of warm-blooded animals.

It is known that when the center of the flexors of one of the limbs is excited, the center of its extensors is inhibited and vice versa. D. Eccles discovered the mechanism of this phenomenon in the following experiment. It irritated the afferent nerve, causing excitation of the motor neuron innervating the extensor muscle.

Nerve impulses, having reached the afferent neuron in the dorsal ganglion, are sent along its axon in the spinal cord along two paths: to the motor neuron innervating the extensor muscle, exciting it, and along the collaterals to the intermediate inhibitory neuron, the axon of which is in contact with the motor neuron innervating the flexor muscle, thus causing inhibition of the antagonistic muscle. This type of inhibition was detected in interneurons at all levels of the central nervous system during the interaction of antagonistic centers. It was called translational postsynaptic inhibition. This type of inhibition coordinates and distributes the processes of excitation and inhibition between nerve centers.

Reversible (antidromic) postsynaptic inhibition (Greek: antidromeo to run in the opposite direction) is the process of nerve cells regulating the intensity of signals received by them according to the principle of negative feedback. It lies in the fact that axonal collaterals of a nerve cell establish synaptic contacts with special interneurons (Renshaw cells), the role of which is to influence neurons that converge on the cell sending these axonal collaterals. This principle is used to inhibit motor neurons.

The occurrence of an impulse in a mammalian motor neuron not only activates muscle fibers, but also activates Renshaw inhibitory cells through axon collaterals. The latter establish synaptic connections with motor neurons. Therefore, increased firing of a motor neuron leads to greater activation of Renshaw cells, causing increased inhibition of motor neurons and a decrease in the frequency of their firing. The term “antidromic” is used because the inhibitory effect is easily caused by antidromic impulses that reflexively arise in motor neurons.

The more excited the motor neuron is, the more strong impulses go to the skeletal muscles along its axon, the more intensely the Renshaw cell is excited, which suppresses the activity of the motor neuron. Consequently, there is a mechanism in the nervous system that protects neurons from excessive excitation. Feature postsynaptic inhibition is that it is suppressed by strychnine and tetanus toxin (these pharmacological substances do not affect excitation processes).

As a result of suppression of postsynaptic inhibition, the regulation of excitation in the central nervous system is disrupted, excitation spreads (“diffuses”) throughout the central nervous system, causing overexcitation of motor neurons and convulsive contractions of muscle groups (convulsions).

Reticular inhibition (lat. reticularis - reticular) is a nervous process developing in spinal neurons under the influence of descending impulses from the reticular formation (the giant reticular nucleus of the medulla oblongata). The effects created by reticular influences are functionally similar to recurrent inhibition developing on motor neurons. The influence of the reticular formation is caused by persistent IPSPs, covering all motor neurons, regardless of their functional affiliation.

In this case, as with recurrent inhibition of motor neurons, their activity is limited. There is a definite interaction between this descending control from the reticular formation and the recurrent inhibitory system through the Renshaw cells, and the Renshaw cells are under constant inhibitory control from the two structures. The inhibitory influence of the reticular formation is an additional factor in regulating the level of activity of motor neurons.

Primary inhibition can be caused by mechanisms of a different nature that are not associated with changes in the properties of the postsynaptic membrane. In this case, inhibition occurs on the presynaptic membrane (synaptic and presynaptic inhibition).

Synaptic inhibition (Greek sunapsis contact, connection) is a nervous process based on the interaction of a transmitter secreted and released by presynaptic nerve endings with specific molecules of the postsynaptic membrane. The excitatory or inhibitory nature of the action of the transmitter depends on the nature of the channels that open in the postsynaptic membrane. Direct proof the presence of specific inhibitory synapses in the central nervous system was first obtained by D. Lloyd (1941).

Data regarding electrophysiological manifestations of synaptic inhibition: presence of synaptic delay, absence electric field in the area of synaptic endings gave reason to consider it a consequence of the chemical action of a special inhibitory mediator secreted by synaptic endings. D. Lloyd showed that if the cell is in a state of depolarization, then the inhibitory transmitter causes hyperpolarization, while against the background of hyperpolarization of the postsynaptic membrane it causes its depolarization.

Presynaptic inhibition(Latin prae - in front of something + Greek sunapsis contact, connection) - a special case of synaptic inhibitory processes, manifested in the suppression of neuron activity as a result of a decrease in the effectiveness of excitatory synapses even at the presynaptic link by inhibiting the process of transmitter release by excitatory nerve endings. In this case, the properties of the postsynaptic membrane do not undergo any changes. Presynaptic inhibition is carried out through special inhibitory interneurons. Its structural basis is axo-axonal synapses formed by the axon terminals of inhibitory interneurons and the axonal endings of excitatory neurons.

In this case, the axon terminal of the inhibitory neuron is presympathetic in relation to the terminal of the excitatory neuron, which turns out to be postsynaptic in relation to the inhibitory ending and presynaptic in relation to the nerve cell activated by it. At the endings of the presynaptic inhibitory axon, a transmitter is released, which causes depolarization of excitatory endings by increasing the permeability of their membrane to CI-. Depolarization causes a decrease in the amplitude of the action potential arriving at the excitatory ending of the axon. As a result, the process of transmitter release by excitatory nerve endings is inhibited and the amplitude of the excitatory postsynaptic potential is reduced.

A characteristic feature of presynaptic depolarization is its slow development and long duration (several hundred milliseconds), even after a single afferent impulse.

Presynaptic inhibition differs significantly from postsynaptic inhibition in pharmacological terms. Strychnine and tetanus toxin do not affect its course. However, narcotic substances (chloralose, Nembutal) significantly enhance and prolong presynaptic inhibition. This type of inhibition is found in various parts of the central nervous system. Most often it is detected in the structures of the brain stem and spinal cord. In the first studies of the mechanisms of presynaptic inhibition, it was believed that the inhibitory effect occurs at a point distant from the soma of the neuron, therefore it was called “remote” inhibition.

The functional significance of presynaptic inhibition, covering the presynaptic terminals through which afferent impulses arrive, is to limit the flow of afferent impulses to the nerve centers. Presynaptic inhibition primarily blocks weak asynchronous afferent signals and allows stronger ones to pass through; therefore, it serves as a mechanism for separating more intense afferent impulses from the general flow. This has a huge adaptive value for the body, since of all the afferent signals going to the nerve centers, the most important, the most necessary for a given specific time are highlighted. Thanks to this, the nerve centers and the nervous system as a whole are freed from processing less essential information.

Secondary inhibition is inhibition carried out by the same nervous structures in which excitation occurs. This nervous process is described in detail in the works of N.E. Vvedensky (1886, 1901).

Reciprocal inhibition (Latin reciprocus - mutual) is a nervous process based on the fact that the same afferent pathways through which one group of nerve cells are excited provide inhibition of other groups of cells through interneurons. Reciprocal relationships of excitation and inhibition in the central nervous system were discovered and demonstrated by N.E. Vvedensky: irritation of the skin on the hind leg of a frog causes it to flex and inhibit flexion or extension on the opposite side. The interaction of excitation and inhibition is common property throughout the nervous system and is found in both the brain and spinal cord. It has been experimentally proven that the normal performance of each natural motor act is based on the interaction of excitation and inhibition on the same neurons of the central nervous system.

General central inhibition is a nervous process that develops during any reflex activity and involves almost the entire central nervous system, including the centers of the brain. General central inhibition usually manifests itself before the onset of any motor reaction. It can manifest itself with such a small force of stimulation that there is no motor effect. This type of inhibition was first described by I.S. Beritov (1937). It provides concentration of excitation of other reflex or behavioral acts that could arise under the influence of stimuli. An important role in the creation of general central inhibition belongs to the gelatinous substance of the spinal cord.

With electrical stimulation of the gelatinous substance in the spinal preparation of a cat, a general inhibition of reflex reactions caused by irritation of the sensory nerves occurs. General inhibition is an important factor in creating the holistic behavioral activity of animals, as well as in ensuring selective excitation of certain working organs.

Parabiotic inhibition develops in pathological conditions when the lability of the structures of the central nervous system decreases or a very massive simultaneous excitation of a large number of afferent pathways occurs, as, for example, during traumatic shock.

Some researchers identify another type of inhibition - inhibition following excitation. It develops in neurons after the end of excitation as a result of strong trace hyperpolarization of the membrane (postsynaptic).

Structure and functions of the sympathetic and parasympathetic divisions of the autonomic nervous system. The place and role of the autonomic nervous system in the regulation of functions. Schemes, examples. Interaction of the autonomic and endocrine systems

The autonomic nervous system is the part of the nervous system that regulates the level of functional activity internal organs, blood and lymphatic vessels, secretory activity of the external and internal secretion glands of the body.

The autonomic (autonomic) nervous system performs adaptive and trophic functions, actively participating in the maintenance homeostasis(i.e. constancy of the environment) in the body. It adapts the functions of internal organs and the entire human body to specific changes in the environment, influencing both physical and mental activity of a person.

Its nerve fibers (usually not all completely covered with myelin) innervate the smooth muscles of the walls of internal organs, blood vessels and skin, glands and heart muscle. Ending in skeletal muscles and skin, they regulate the level of metabolism in them, providing them with nutrition (trophism). The influence of the VNS also extends to the degree of receptor sensitivity. Thus, the autonomic nervous system covers more extensive areas of innervation than the somatic one, since the somatic nervous system innervates only the skin and skeletal muscles, and the ANS regulates all internal organs and all tissues, carrying out adaptive-trophic functions in relation to everything body, including skin and muscles.

The structure of the autonomic nervous system differs from the somatic one. The fibers of the somatic nervous system always leave the central nervous system (spinal cord and brain) and go, without interruption, to the innervated organ. And they are completely covered by the myelin sheath. The somatic nerve is thus formed only by the processes of neurons whose bodies lie in the central nervous system. As for the nerves of the ANS, they are always formed two neurons.

One is central, lies in the spinal cord or brain, the second (effector) is in the autonomic ganglion, and the nerve consists of two sections - preganglionic, usually covered with a myelin sheath and therefore white, and postganglionic - not covered with a myelin sheath and therefore gray in color. Their autonomic ganglia (always located on the periphery from the central nervous system) are located in three places. First ( paravertebral ganglia) - in the sympathetic nerve chain located on the sides of the spine; the second group - more distant from the spinal cord - prevertebral, and, finally, the third group - in the walls of innervated organs ( intramural).

Some authors also highlight extramural ganglia that lie not in the wall, but close to the innervated organ. The further the ganglia are located from the central nervous system, the more of the autonomic nerve is covered with a myelin sheath. And, therefore, the speed of nerve impulse transmission in this part of the autonomic nerve is higher.

The next difference is that the work of the somatic nervous system, as a rule, can be controlled by consciousness, but the ANS cannot. We can basically control the work of skeletal muscles, but we cannot control the contraction of smooth muscles (for example, intestines). Unlike the somatic one, it does not have such a sparse segmentation in innervation. Nerve fibers of the ANS exit the central nervous system from its three sections - the brain, thoracolumbar and sacral sections of the spinal cord.

The reflex arcs of the ANS differ in their structure from the reflex arcs of somatic reflexes. The reflex arc of the somatic nervous system always passes through the central nervous system. As for the ANS, its reflexes can be carried out both through long arcs (through the central nervous system) and through short ones - through the autonomic ganglia. Short reflex arcs passing through the autonomic ganglia have great importance, because provide urgent adaptive reactions of innervated organs that do not require the participation of the central nervous system.

Braking- an active process that occurs when stimuli act on tissue, manifests itself in the suppression of other excitation, there is no functional function of the tissue.

Inhibition can develop only in the form of a local response.

There are two types of braking:

1) primary. For its occurrence it is necessary to have special inhibitory neurons. Inhibition occurs primarily without previous excitation under the influence of inhibitory mediator .

There are two types of primary inhibition:

- presynaptic at the axo-axonal synapse;

- postsynaptic at the axodendritic synapse.

2) secondary. It does not require special inhibitory structures, occurs as a result of changes in the functional activity of ordinary excitable structures, and is always associated with the process of excitation.

Types of secondary braking:

- transcendental, which occurs when there is a large flow of information entering the cell. The flow of information lies beyond the functionality of the neuron;

- pessimal, which occurs with a high frequency of irritation; parabiotic, which occurs with strong and long-lasting irritation;

Inhibition following excitation, resulting from a decrease in the functional state of neurons after excitation;

Braking based on the principle of negative induction;

Inhibition of conditioned reflexes.

The processes of excitation and inhibition are closely related to each other, occur simultaneously and are different manifestations of a single process. Foci of excitation and inhibition are mobile, cover larger or smaller areas of neuronal populations and can be more or less pronounced. Excitation is certainly replaced by inhibition, and vice versa, that is, there is an inductive relationship between inhibition and excitation.

Braking lies in basis coordination of movements, protects central neurons from overexcitation. Inhibition in the central nervous system can occur when nerve impulses of varying strength from several stimuli simultaneously enter the spinal cord. Stronger stimulation inhibits reflexes that should have occurred in response to weaker ones.

In 1862 I.M. Sechenov discovered phenomenon central braking. He proved in his experiment that irritation with a sodium chloride crystal of the visual thalamus of a frog (the cerebral hemispheres have been removed) causes inhibition of spinal cord reflexes. After the stimulus was removed, the reflex activity of the spinal cord was restored. The result of this experiment allowed I.M. Secheny to conclude that in the central nervous system, along with the process of excitation, a process of inhibition develops, which is capable of inhibiting the reflex acts of the body. N. E. Vvedensky suggested that the phenomenon of inhibition is based on the principle of negative induction: a more excitable area in the central nervous system inhibits the activity of less excitable areas.

Modern interpretation of the experience of I. M. Sechenov(I.M. Sechenov irritated the reticular formation of the brain stem): excitation of the reticular formation increases the activity of inhibitory neurons of the spinal cord - Renshaw cells, which leads to inhibition of α-motoneurons of the spinal cord and inhibits the reflex activity of the spinal cord.

Inhibitory synapses formed by special inhibitory neurons (more precisely, their axons). The mediator may be glycine, GABA and a number of other substances. Typically, glycine is produced at synapses through which postsynaptic inhibition occurs. When glycine as a mediator interacts with glycine receptors of a neuron, hyperpolarization of the neuron occurs ( TPSP ) and, as a consequence, a decrease in the excitability of the neuron up to its complete refractoriness. As a result, the excitatory influences exerted through other axons become ineffective or ineffective. The neuron shuts down completely.

Inhibitory synapses open mainly chlorine channels, allowing chloride ions to easily pass through the membrane. To understand how inhibitory synapses inhibit a postsynaptic neuron, we need to remember what we know about the Nernst potential for Cl- ions. We calculated it to be approximately -70 mV. This potential is more negative than the resting membrane potential of the neuron, equal to -65 mV. Consequently, the opening of chloride channels will promote the movement of negatively charged Cl- ions from the extracellular fluid inward. This shifts the membrane potential towards more negative values compared to rest to approximately -70 mV.

The opening of potassium channels allows positively charged K+ ions to move outward, resulting in greater negativity inside the cell than at rest. Thus, both events (the entry of Cl- ions into the cell and the exit of K+ ions from it) increase the degree of intracellular negativity. This process is called hyperpolarization. An increase in the negativity of the membrane potential compared to its intracellular level at rest inhibits the neuron, therefore the deviation of the negative values beyond the limits of the initial resting membrane potential is called TPSP.

Functional Features somatic and autonomic nervous system. Comparative characteristics sympathetic, parasympathetic and metasympathetic divisions of the autonomic nervous system.

The first and main difference The structure of the ANS from the structure of the somatic consists in the location of the efferent (motor) neuron. In the SNS, intercalary and motor neurons are located in the gray matter of the SC; in the ANS, the effector neuron is moved to the periphery, beyond the SC, and lies in one of the ganglia - para-, prevertebral or intraorgan. Moreover, in the metasympathetic part of the ANS, the entire reflex apparatus is located entirely in the intramural ganglia and nerve plexuses of the internal organs.

The second difference concerns exit of nerve fibers from the central nervous system. Somatic NVs leave the SC segmentally and cover at least three adjacent segments with innervation. The fibers of the ANS emerge from three sections of the central nervous system (GM, thoracolumbar and sacral sections of the SM). They innervate all organs and tissues without exception. Most visceral systems have a triple (sympathetic, para- and metasympathetic) innervation.

The third difference concerns innervation of somatic and ANS organs. Transection of the ventral roots of the SC in animals is accompanied by complete degeneration of all somatic efferent fibers. It does not affect the arc of the autonomic reflex due to the fact that its effector neuron is located in the para- or prevertebral ganglion. Under these conditions, the effector organ is controlled by the impulses of a given neuron. It is this circumstance that emphasizes the relative autonomy of this department of the National Assembly.

The fourth difference concerns to the properties of nerve fibers. In the ANS, they are mostly pulpless or thin pulpy, such as preganglionic fibers, the diameter of which does not exceed 5 μm. Such fibers belong to type B. Postganglionic fibers are even thinner, most of them are devoid of a myelin sheath, they belong to type C. In contrast, somatic efferent fibers are thick, pulpy, their diameter is 12-14 microns. In addition, pre- and postganglionic fibers are characterized by low excitability. To evoke a response in them, a much greater force of irritation is required than for somatic motor fibers.

ANS fibers are characterized by a long refractory period and long chronaxy. The speed of NI propagation along them is low and is up to 18 m/s in preganglionic fibers, and up to 3 m/s in postganglionic fibers. Action potentials of ANS fibers are characterized by a longer duration than in somatic efferents. Their occurrence in preganglionic fibers is accompanied by a long trace positive potential, in postganglionic fibers - a trace negative potential followed by a long trace hyperpolarization (300-400 ms).

VNS provides extraorgan and intraorgan regulation of body functions and includes three components:

1) sympathetic;

2) parasympathetic;

3) methsympathetic.

The autonomic nervous system has a number of anatomical and physiological features that determine the mechanisms of its operation.

Anatomical properties:

1. Three-component focal arrangement of nerve centers. The lowest level of the sympathetic department is represented by the lateral horns from the VII cervical to the III-IV lumbar vertebrae, and the parasympathetic - by the sacral segments and the brain stem. The higher subcortical centers are located on the border of the hypothalamic nuclei (the sympathetic department is the posterior group, and the parasympathetic division is the anterior group). The cortical level lies in the area of the sixth to eighth fields Brodman(motosensory zone), in which point localization of incoming nerve impulses is achieved. Due to the presence of such a structure of the autonomic nervous system, the work of the internal organs does not reach the threshold of our consciousness.

2. Availability autonomic ganglia. In the sympathetic department, they are located either on both sides along the spine, or are part of the plexuses. Thus, the arch has a short preganglionic and a long postganglionic path. The neurons of the parasympathetic division are located near the working organ or in its wall, so the arc has a long preganglionic and short postganglionic path.

3. Effetor fibers belong to groups B and C.

Physiological properties:

1. Features of the functioning of the autonomic ganglia. Presence of a phenomenon animations(simultaneous occurrence of two opposite processes - divergence and convergence). Divergence- divergence of nerve impulses from the body of one neuron to several postganglionic fibers of another. Convergence- convergence on the body of each postganglionic neuron of impulses from several preganglionic ones.

This ensures the reliability of the transfer of information from the central nervous system to the working organ. An increase in the duration of the postsynaptic potential, the presence of trace hyperpolarization and synoptic delay contribute to the transmission of excitation at a speed of 1.5-3.0 m/s. However, the impulses are partially extinguished or completely blocked in the autonomic ganglia. In this way they regulate the flow of information from the central nervous system. Due to this property, they are called nerve centers located on the periphery, and the autonomic nervous system is called autonomous.

2. Features of nerve fibers. Preganglionic nerve fibers belong to group B and conduct excitation at a speed of 3-18 m/s, postganglionic nerve fibers belong to group C. They conduct excitation at a speed of 0.5-3.0 m/s. Since the efferent pathway of the sympathetic department is represented by preganglionic fibers, and the parasympathetic one is represented by postganglionic fibers, the speed of impulse transmission is higher in the parasympathetic nervous system.

Thus, the autonomic nervous system functions differently, its work depends on the characteristics of the ganglia and the structure of the fibers.

Sympathetic nervous system innervates all organs and tissues (stimulates the heart, increases the lumen of the respiratory tract, inhibits the secretory, motor and absorption activity of the gastrointestinal tract, etc.). It performs homeostatic and adaptive-trophic functions.

Her homeostatic role is to maintain consistency internal environment the body is in an active state, i.e. the sympathetic nervous system is activated only during physical activity, emotional reactions, stress, pain, and blood loss.

Adaptation-trophic function aimed at regulating the intensity of metabolic processes. This ensures the body's adaptation to changing environmental conditions.

Thus, the sympathetic department begins to act in an active state and ensures the functioning of organs and tissues.

Parasympathetic nervous system is an antagonist of the sympathetic and performs homeostatic and protective functions, regulates the emptying of hollow organs.

The homeostatic role is restorative in nature and acts in a state of rest. This manifests itself in the form of a decrease in the frequency and strength of heart contractions, stimulation of the gastrointestinal tract with a decrease in blood glucose levels, etc.

All protective reflexes rid the body of foreign particles. For example, coughing clears the throat, sneezing clears the nasal passages, vomiting removes food, etc.

Emptying of hollow organs occurs when the tone of the smooth muscles that make up the wall increases. This leads to the entry of nerve impulses into the central nervous system, where they are processed and sent along the effector pathway to the sphincters, causing them to relax.

Metsympathetic nervous system is a collection of microganglia located in organ tissue. They consist of three types of nerve cells - afferent, efferent and intercalary, therefore they perform the following functions:

Provides intraorgan innervation;

They are an intermediate link between the tissue and the extraorgan nervous system. When exposed to a weak stimulus, the metosympathetic department is activated, and everything is decided at the local level. When strong impulses arrive, they are transmitted through the parasympathetic and sympathetic divisions to the central ganglia, where they are processed.

The methsympathetic nervous system regulates the functioning of smooth muscles that make up most organs of the gastrointestinal tract, myocardium, secretory activity, local immunological reactions, etc.

The role of the SM in the processes of regulation of the activity of the musculoskeletal system and the vegetative functions of the body. Characteristics of spinal animals. Principles of the spinal cord. Clinically important spinal reflexes.

SM is the most ancient formation of the central nervous system. A characteristic feature of the structure is segmentarity.

SM neurons form it Gray matter in the form of anterior and posterior horns. They perform the reflex function of the SC.

Hind horns contain neurons ( interneurons), which transmit impulses to the overlying centers, to the symmetrical structures of the opposite side, to the anterior horns of the spinal cord. The dorsal horns contain afferent neurons that respond to pain, temperature, tactile, vibration, and proprioceptive stimuli.

Front horns contain neurons ( motor neurons), giving axons to the muscles, they are efferent. All descending paths CNS motor reactions end in the anterior horns.

IN lateral horns The neurons of the sympathetic division of the autonomic nervous system are located in the cervical and two lumbar segments, and the parasympathetic ones are located in the second to fourth segments.

The SC contains many interneurons that provide communication with the segments and with the overlying parts of the central nervous system; they account for 97% of the total number of spinal cord neurons. They include associative neurons - neurons of the SC's own apparatus; they establish connections within and between segments.

White matter The SM is formed by myelin fibers (short and long) and plays a conductive role.

Short fibers connect neurons of the same or different segments of the spinal cord.

Long fibers (projection) form the pathways of the spinal cord. They form ascending pathways to the brain and descending pathways from the brain.

The spinal cord performs reflex and conductive functions.

Reflex function allows you to realize all motor reflexes of the body, reflexes of internal organs, thermoregulation, etc. Reflex reactions depend on the location, strength of the stimulus, the area of the reflexogenic zone, the speed of impulse transmission along the fibers, and the influence of the brain.

Reflexes are divided into:

1) exteroceptive(occur when irritated by agents external environment sensory stimuli);

2) interoceptive(occur when irritation of presso-, mechano-, chemo-, thermoreceptors): viscero-visceral - reflexes from one internal organ to another, viscero-muscular - reflexes from internal organs to skeletal muscles;

3) proprioceptive(own) reflexes from the muscle itself and the formations associated with it. They have a monosynaptic reflex arc. Proprioceptive reflexes regulate motor activity due to tendon and postural reflexes. Tendon reflexes (knee, Achilles, triceps brachii, etc.) occur when muscles are stretched and cause relaxation or contraction of the muscle, occurring with every muscle movement;

4) posotonic reflexes (occur when vestibular receptors are excited when the speed of movement and position of the head relative to the body changes, which leads to a redistribution of muscle tone (increased extensor tone and decreased flexor tone) and ensures body balance).

The study of proprioceptive reflexes is carried out to determine the excitability and degree of damage to the central nervous system.

Conductor function ensures communication of SC neurons with each other or with overlying parts of the central nervous system.

Spinal animal- an animal in which the spinal column is crossed, often at the level of the neck, but the function of most of the spinal column is preserved;

Immediately after transection of the SC, most of its functions below the point of intersection in the spinal animal are sharply inhibited. After a few hours (in rats and cats) or several days, weeks (in monkeys), most of the functions characteristic of the spinal cord are restored almost to normal, providing the possibility of experimental study of the drug.

Inhibition in the central nervous system is an active nervous process, the result of which is the cessation or weakening of excitation (Sechenov, 1863).

Goltz (1870) - discovered the manifestation of inhibition in the spinal frog.

Megun (1944) found that stimulation of the medial part of the RF of the medulla oblongata inhibits the reflex activity of the spinal cord

BRAKING PROCESSES

IN THE CENTRAL NERVOUS SYSTEM

Along with the mechanisms of excitation in the central nervous system, there are also mechanisms of inhibition, which manifest themselves in the cessation or reduction of the activity of nerve cells. In contrast to excitation, inhibition is a local, non-propagating process that occurs on the cell membrane. Sechenov braking. The presence of an inhibition process in the central nervous system was first shown by I.M. Sechenov in 1862 in experiments on a frog. A section was made in the frog's brain at the level of the visual thalamus and the withdrawal reflex time was measured. hind paw when immersing it in a solution of sulfuric acid (Turk method). When a crystal is applied to the section of the visual tuberosities table salt reflex time

increased. Cessation of the effect of salt on the visual thalamus led to the restoration of the original reflex reaction time. The Shdershian paw reflex is caused by excitation of the spinal centers. A crystal of salt, irritating the visual tuberosities, causes excitement, which spreads to the spinal centers and inhibits their activity. THEM. Sechenov came to the conclusion that inhibition is a consequence of the interaction of two or more excitations on the neurons of the central nervous system. In this case, one excitation inevitably becomes inhibited, and the other - inhibitory. Suppression by one

excitation of another occurs both at the level of postsynaptic membranes

(postsynaptic inhibition), and due to a decrease in the effectiveness of excitatory synapses at the presynaptic level (presynaptic inhibition).

Presynaptic inhibition. Presynantic inhibition develops in the presynaptic part

synapse due to the action of axo-axonal synapses on its membrane. As a result of both depolarizing and hyperpolarizing effects, conduction is blocked

excitation impulses along presynaptic pathways to the gustsinaitic nerve cell.

Postsynaptic inhibition. The most widespread mechanism in the central nervous system is post-inaptic

inhibition, which is carried out by special inhibitory intercalary nerve cells, for example, Renshaw cells in the spinal cord or Purknier cells (piriform neurons) in the cerebellar cortex]. The peculiarity of inhibitory nerve cells is that their synapses contain mediators that cause IPSP on the postsynaptic membrane of the neuron, i.e. short-term hyperpolarization. For example, for motor neurons of the spinal cord the hyperpolarizing transmitter is the amino acid glycine, and for many cortical neurons big brain such a mediator is gamma-aminobutyric acid -

GABA. A special case of postsynaptic inhibition is recurrent inhibition.

Reciprocal inhibition. The mechanism of postsynaptic inhibition underlies such types of inhibition as reciprocal and lateral. Reciprocal inhibition is one of the physiological mechanisms for coordinating the activity of nerve centers. Thus, the inhalation and exhalation centers, pressor and depressor vasomotor centers in the medulla oblongata are alternately reciprocally inhibited.

Lateral inhibition. With lateral inhibition, the activity of neurons or receptors located next to the excited neurons or receptors stops. The mechanism of lateral inhibition provides the discriminatory ability of analyzers. Thus, in the auditory analyzer, lateral inhibition ensures discrimination of the frequency of sounds; in the visual analyzer, lateral inhibition sharply increases the contrast of the contours of the perceived image, and in

tactile analyzer helps differentiate two points of touch.

The role of inhibition

1) Both types of inhibition with all their varieties play a protective role (the absence would lead to the depletion of transmitters in the axons of neurons and the cessation of central nervous system activity);

2) Plays important role in processing information entering the central nervous system;

3) Ensuring the coordination activities of the central nervous system.

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Ticket 15. History of the study of inhibition. Sechenov's experience.

The phenomenon of central inhibition was discovered by I.M. Sechenov in 1362 guide. He removed the frog's brain hemispheres and determined the time of the spinal reflex to irritation of the paw with sulfuric acid. Then to the thalamus, i.e. applied a crystal of table salt to the visual tuberosities and found that the reflex time increased significantly. This indicated inhibition of the reflex. Sechenov concluded that the overlying N.Ts. during hypnotic excitation, the underlying ones are inhibited. Inhibition in the central nervous system prevents the development of excitation or weakens ongoing excitation. An example of inhibition can be the cessation of a reflex reaction against the background of the action of another stronger stimulus. Initially, a unitary-chemical theory of inhibition was proposed. It was based on Dale's principle: one neuron, one transmitter. According to it, inhibition is provided by the same neurons and synapses as excitation. Subsequently, the correctness of the binary chemical theory was proven. In accordance with the latter, inhibition is provided by special inhibitory neurons, which are intercalary. These are Renshaw cells of the spinal cord and Purkinje neurons. Inhibition in the central nervous system is necessary for the integration of neurons into a single nerve center.

Ticket 16. Braking, its types, mechanisms and

Functional meaning.

Braking- an active nervous process caused by excitation and manifested in the suppression or prevention of another wave of excitation. Ensures (together with stimulation) the normal functioning of all organs and the body as a whole. It has a protective value (primarily for the nerve cells of the cerebral cortex), protecting the nervous system from overexcitation.

Central braking discovered in 1863 by I.M. Sechenov.

Primary inhibition

Primary inhibition occurs in special inhibitory cells adjacent to the inhibitory neuron. In this case, inhibitory neurons release the corresponding neurotransmitters.

Types: 1) Postsynaptic - the main type of primary inhibition, caused by excitation of Renshaw cells and interneurons. With this type of inhibition, hyperpolarization of the postsynaptic membrane occurs, which causes inhibition.

Examples of primary inhibition:

Reciprocal - a neuron affects a cell, which in response inhibits the same neuron.

Reciprocal inhibition is mutual inhibition, in which the excitation of one group of nerve cells provides inhibition of other cells through an interneuron.

Lateral - the inhibitory cell inhibits nearby neurons. Similar phenomena develop between bipolar and ganglion cells of the retina, which creates conditions for a clearer vision of the object.

Return relief is the neutralization of neuron inhibition when inhibitory cells are inhibited by other inhibitory cells.

Presynaptic - occurs in ordinary neurons and is associated with the process of excitation.

Secondary braking Secondary inhibition occurs in the same neurons that generate excitation.

Types of secondary braking:

Pessimal inhibition- this is secondary inhibition that develops in excitatory synapses as a result of strong depolarization of the postsynaptic membrane under the influence of multiple impulses.

Inhibition following excitation occurs in ordinary neurons and is also associated with the excitation process. At the end of the act of excitation of a neuron, a strong trace hyperpolarization can develop in it. At the same time, the excitatory postsynaptic potential cannot bring membrane depolarization to a critical level of depolarization, voltage-gated sodium channels do not open and an action potential does not arise.

Peripheral inhibition-Conditioned and unconditional inhibition

The terms “conditioned” and “unconditioned” inhibition were proposed by I. P. Pavlov.

Conditioned, or internal, inhibition is a form of inhibition of the conditioned reflex that occurs when conditioned stimuli are not reinforced by unconditioned ones. Conditioned inhibition is an acquired property and is developed during ontogenesis.

Classification of types of central inhibition. Primary and secondary

Conditioned inhibition is central inhibition and weakens with age.

Unconditional (external) inhibition- inhibition of a conditioned reflex that occurs under the influence of unconditioned reflexes (for example, an orienting reflex). I.P. Pavlov attributed unconditional inhibition to the innate properties of the nervous system, that is, unconditional inhibition is a form of central inhibition.

Inhibition in the central nervous system (I.M. Sechenov). Presynaptic and postsynaptic inhibition. Inhibitory neurons and transmitters. The importance of inhibition in nervous activity. C21-22

Methods of physiological research (observation, acute experience and chronic experiment). Contribution of domestic and foreign physiologists to the development of physiology. C 1-2

The connection between physiology and the disciplines: chemistry, biochemistry, morphology, psychology, pedagogy and the theory and methodology of physical education. C 3

Basic properties of living formations: interaction with environment, metabolism and energy, excitability and arousal, stimuli and their classification, homeostasis. C 3-4

Membrane potentials – resting potential, local potential, action potential, their origin and properties. Specific manifestations of excitement. C 4-6

Excitability parameters. Threshold of irritation strength (rheobase). Chronaxia. Changes in excitability during excitement, functional lability. C 6-8

General characteristics of the organization and functions of the central nervous system (CNS). C 8-9

The concept of reflex. Reflex arc and feedback (reflex ring).

Carrying out excitation along a reflex arc, reflex time. From 9-11

Nervous and humoral mechanisms of regulation of functions in the body and their interaction. From 11-13

Neuron: structure, functions and classification of neurons. Features of the conduction of nerve impulses along axons. From 13-14

Synapse structure. Mediators. Synaptic transmission of nerve impulses. 15-17

The concept of the nerve center. Features of the conduction of excitation through nerve centers (unilateral conduction, slow conduction, summation of excitation, transformation and assimilation of rhythm). From 17-18

The summation of excitation in CNS neurons is temporal and spatial. Background and evoked impulse activity of neurons. Trace processes under the influence of muscle activity. From 18-21

Inhibition in the central nervous system (I.M. Sechenov). Presynaptic and postsynaptic inhibition. Inhibitory neurons and transmitters. Braking value in nervous activity. C21-22

15. General plan of the structure and functions of sensory systems. Mechanism of receptor excitation (generator potential). from 23

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Central inhibition (primary) is a nervous process that occurs in the central nervous system and leads to the weakening or prevention of excitation. According to modern concepts, central inhibition is associated with the action of inhibitory neurons or synapses that produce inhibitory mediators (glycine, gamma-aminobutyric acid), which cause a special type of electrical changes on the postsynaptic membrane called inhibitory postsynaptic potentials (IPSPs) or depolarization of the presynaptic nerve ending with which another one is in contact nerve ending of an axon.

Therefore, central (primary) postsynaptic inhibition and central (primary) presynaptic inhibition are distinguished.

Presynaptic inhibition (Latin prae - in front of something + Greek sunapsis contact, connection) is a special case of synaptic inhibitory processes, manifested in the suppression of neuron activity as a result of a decrease in the effectiveness of excitatory synapses even at the presynaptic link by inhibiting the process of transmitter release by excitatory nerve endings . In this case, the properties of the postsynaptic membrane do not undergo any changes. Presynaptic inhibition is carried out through special inhibitory interneurons. Its structural basis is axo-axonal synapses formed by the axon terminals of inhibitory interneurons and the axonal endings of excitatory neurons.

The functional significance of presynaptic inhibition, covering the presynaptic terminals through which afferent impulses arrive, is to limit the flow of afferent impulses to the nerve centers. Presynaptic inhibition primarily blocks weak asynchronous afferent signals and allows stronger ones to pass through; therefore, it serves as a mechanism for separating more intense afferent impulses from the general flow. This has enormous adaptive significance for the body, since of all the afferent signals going to the nerve centers, the most important, the most necessary for a given specific time are highlighted. Thanks to this, the nerve centers and the nervous system as a whole are freed from processing less essential information.

29. Secondary braking. Its types. Mechanism of occurrence. Principles of coordination activity of the central nervous system (convergence, common end point, divergence, irradiation, reciprocity, dominant).

Secondary. It does not require special inhibitory structures, occurs as a result of changes in the functional activity of ordinary excitable structures, and is always associated with the process of excitation. Types of secondary braking:

a) transcendental, which occurs when there is a large flow of information entering the cell. The flow of information lies outside the limits of the neuron’s performance; b) pessimal, which occurs at a high frequency of stimulation;

c) parabiotic, which occurs during strong and long-term irritation;

d) inhibition following excitation, resulting from a decrease in the functional state of neurons after excitation; e) inhibition according to the principle of negative induction; f) inhibition of conditioned reflexes.

Inhibition underlies the coordination of movements and protects central neurons from overexcitation. Inhibition in the central nervous system can occur when nerve impulses of varying strength from several stimuli simultaneously enter the spinal cord. Stronger stimulation inhibits reflexes that should have occurred in response to weaker ones.

Coordination activity (CA) of the CNS is the coordinated work of CNS neurons, based on the interaction of neurons with each other.

CD functions:

1) ensures the precise performance of certain functions and reflexes; 2) ensures the consistent inclusion of various nerve centers in the work to ensure complex forms of activity 3) ensures the coordinated work of various nerve centers (during the act of swallowing, the breath is held at the moment of swallowing; when the swallowing center is excited, the breathing center is inhibited) .

Basic principles of CNS CD and their neural mechanisms.

1. The principle of irradiation (propagation). When small groups of neurons are excited, the excitation spreads to a significant number of neurons.

2. The principle of convergence. When a large number of neurons are excited, the excitation may converge to one group of nerve cells.3. The principle of reciprocity is the coordinated work of nerve centers, especially in opposite reflexes (flexion, extension, etc.).

4. The principle of dominance. Dominant - the dominant focus of excitation in the central nervous system in this moment. This is the center of persistent, unwavering, non-spreading excitation.

According to I.P. Pavlov’s definition, excitation and inhibition are two sides of the same process. The coordination activity of the central nervous system ensures clear interaction between individual nerve cells and individual groups of nerve cells. There are three levels of integration.

The first level is ensured due to the fact that impulses from different neurons can converge on the body of one neuron, resulting in either summation or a decrease in excitation.

The second level provides interactions between individual groups of cells.

The third level is provided by cells of the cerebral cortex, which contribute to a more advanced level of adaptation of the activity of the central nervous system to the needs of the body.

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The phenomenon of central inhibition was discovered by I.M. Sechenov in 1862. He discovered that if a crystal of table salt is applied to a cross-section of the visual tubercles of a frog or a weak electric current is applied, then the time of the Turk reflex sharply lengthens (Turk reflex - flexion of the paw when immersing it y to acid). Soon new facts were discovered demonstrating the phenomena of inhibition in the central nervous system. Goltz showed that the Türk reflex is inhibited when the other paw is compressed with tweezers; Sherrington proved the presence of inhibition of the reflex contraction of the extensor during the flexion reflex. It has been proven that the intensity of reflex inhibition depends on the ratio of the strength of the exciting and inhibitory stimuli.

In the central nervous system, there are several methods of inhibition, having different natures and different localizations. but in principle based on one mechanism - an increase in the difference between the critical level of depolarization and the value of the membrane potential of neurons.

1. Postsynaptic inhibition. Inhibitory neurons . It has now been established that in the central nervous system, along with excitatory neurons, there are also special inhibitory neurons. An example is the so-called Renshaw cell in the spinal cord. Renshaw discovered that the axons of motor neurons, before leaving the spinal cord, give rise to one or more collaterals that end on special cells, whose axons form inhibitory synapses on the motor neurons of a given segment. Due to this, the excitation that occurs in the motor neuron spreads along the direct path to the periphery to the skeletal muscle, and along the collateral activates the inhibitory cell, which suppresses further excitation of the motor neuron. This is a mechanism that automatically protects nerve cells from excessive stimulation. Inhibition carried out with the participation of Renshaw cells is called recurrent postsynaptic inhibition. The inhibitory transmitter in the Renshaw cell is glycine.

The nerve impulses that arise when inhibitory neurons are excited do not differ from the action potentials of ordinary excitatory neurons. However, in the nerve endings of inhibitory neurons, under the influence of this impulse, a transmitter is released, which does not depolarize, but, on the contrary, hyperpolarizes the postsynaptic membrane. This hyperpolarization is recorded in the form of an inhibitory postsynaptic potential (IPSP), an electropositive wave. IPSP weakens the excitatory potential and thereby prevents the achievement of the critical level of membrane depolarization necessary for the occurrence of spreading excitation. Postsynaptic inhibition can be eliminated by strychnine, which blocks inhibitory synapses.

2.Post-tetanic inhibition. A special type of inhibition is that which occurs if, after the end of excitation, a strong hyperpolarization of the membrane occurs in the cell. The excitatory postsynaptic potential under these conditions is insufficient for critical depolarization of the membrane and the generation of spreading excitation. The reason for this inhibition is that trace potentials are capable of summation, and after a series of frequent impulses, a summation of a positive trace potential occurs.

3.Pessimal inhibition. Inhibition of the activity of a nerve cell can be carried out without the participation of special inhibitory structures. In this case, it occurs in excitatory synapses as a result of strong depolarization of the postsynaptic membrane under the influence of too frequent impulses (like pessimum in a neuromuscular preparation).

Intermediate neurons of the spinal cord and neurons of the reticular formation are especially prone to pessimal inhibition. With persistent depolarization, a state similar to Verigo's cathodic depression occurs.

4.Presynaptic inhibition. It was discovered in the central nervous system relatively recently, so it has been studied less. Presynaptic inhibition is localized in presynaptic terminals in front of the synaptic plaque. The presynaptic terminals contain the endings of the axons of other nerve cells, which form axo-axonal synapses here. Their mediators depolarize the terminal membrane and lead to a state similar to Verigo’s cathodic depression. This causes a partial or complete blockade of the conduction of exciting impulses along the nerve fibers going to the nerve endings. Presynaptic inhibition is usually long lasting.

Braking classification-

1. Primary inhibition – specialized inhibitory neurons with special transmitters (GABA, glycine) a- postsynaptic b-presynaptic

2. Secondary inhibition - in excitatory synapses in a certain state a) pessimal b) after excitation

Inhibition in the central nervous system. Inhibitory neurons. Inhibitory synapses. The mechanism of occurrence of inhibitory postsynaptic potential (IPSP). Inhibitory mediators and their receptors. Interaction of EPSP and IPSP on a neuron. The role of inhibition in the central nervous system.

Integrative and coordination activity of central nervous formations is carried out with the obligatory participation of inhibitory processes.

Inhibition in the central nervous system is an active process, manifested externally in the suppression or weakening of the excitation process and characterized by a certain intensity and duration.

Inhibition is normally inextricably linked with excitation, is its derivative, accompanies the excitatory process, limiting and preventing the excessive spread of the latter. In this case, inhibition often limits excitation and, together with it, forms a complex mosaic of activated and inhibited zones in the central nerve structures. The formative effect of the inhibitory process develops in space and time. Inhibition is an innate process that is constantly improved during the individual life of the organism.

If the force of the factor causing inhibition is significant, it can spread over a significant space, involving large populations of nerve cells in the inhibitory process.

The history of the development of the doctrine of inhibitory processes in the central nervous system begins with the discovery by I.M. Sechenov of the effect central braking(chemical irritation of the visual thalamus inhibits simple spinal unconditioned reactions). Initially, the assumption of the existence of specific inhibitory neurons that have the ability to exert inhibitory influences on other neurons with which there are synaptic contacts was dictated by a logical necessity to explain the complex forms of coordination activity of the central nervous formations. Subsequently, this assumption found direct experimental confirmation (Eccles, Renshaw), when the existence of special interneurons with synaptic contacts with motor neurons was shown. Activation of these interneurons naturally led to inhibition of motor neurons. Depending on the neural mechanism and the method of inducing the inhibitory process in the central nervous system, several types of inhibition are distinguished: postsynaptic, presynaptic, pessimal.

Postsynaltic inhibition- the main type of inhibition that develops in the postsynaptic membrane of axosomatic and axodendritic synapses under the influence of activation of inhibitory neurons, in the terminal branches of the axonal processes of which the inhibitory transmitter is released and enters the synaptic cleft. The inhibitory effect of such neurons is determined by the specific nature of the mediator - a chemical carrier of a signal from one cell to another. The most common inhibitory neurotransmitter is gamma-aminobutyric acid (GABA). The chemical action of GABA causes a hyperpolarization effect in the postsynaptic membrane in the form of inhibitory postsynaptic potentials (IPSPs), the spatiotemporal summation of which increases the level of membrane potential (hyperpolarization) and leads to a slowdown or complete cessation of the generation of propagating APs.

Return braking called inhibition (suppression) of neuron activity caused by the recurrent collateral of the axon of a nerve cell. Thus, the motor neuron of the anterior horn of the spinal cord, before leaving the spinal cord, gives off a lateral (recurrent) branch, which returns back and ends on inhibitory neurons (Renshaw cells). The axon of the latter ends on motor neurons, exerting an inhibitory effect on them.

Presynaptic inhibition unfolds in axoaxonal synapses, blocking the spread of excitation along the axon.

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Patterns of excitation and processes

The simplest nerve center is a nerve chain consisting of three neurons connected in series (Fig.). Neurons of complex nerve centers have numerous connections among themselves, forming three types of nerve networks:

1. Hierarchical. If the excitement spreads to everything large quantity neurons, then this phenomenon is usually called divergence (Fig.). If, on the contrary, paths go from several neurons to a smaller number, such a mechanism is usually called convergence (Fig.). For example, one motor neuron can be approached by nerve endings from several afferent neurons. In such networks, the outgoing neurons control the underlying ones.

2. Local networks. Contain neurons with short axons. Οʜᴎ provide communication between neurons of one level of the central nervous system and short-term storage of information at this level. An example of them is a ring chain (Fig.). Excitation circulates along such circuits for a certain time. Such circulation is usually called reverberation of excitation (mechanics of short-term memory).

3. Divergent networks with one input. They have one neuron, ᴛ.ᴇ. the entrance forms a large number of connections with neurons of many centers.

Due to the presence of numerous connections between the neurons of the network, irradiation of excitation may occur in them. This is its spread to all neurons.

As a result of irradiation, excitation can move to other nerve centers and even cover the entire nervous system.

Nerve networks contain a large number of interneurons, some of which are inhibitory. For this reason, several types of inhibitory processes may occur in them:

1. Reciprocal inhibition. In this case, signals coming from afferent neurons excite some neurons, but at the same time, through intercalary inhibitory neurons, inhibit others. Such braking is also called conjugate (Fig).

2. Return braking. In this case, excitation goes from the neuron along the axon to another cell. But at the same time along collaterals (branches) to the inhibitory neuron, which forms a synapse on the body of the same neuron. Special case such inhibition is Renshaw inhibition. When motor neurons of the spinal cord are excited, nerve impulses travel along their axons to muscle fibers, but at the same time they spread along the collaterals of this axon to Renshaw cells. Renshaw cell axons form inhibitory synapses on the cell bodies of these same motor neurons. As a result, the more strongly the motor neuron is excited, the stronger the inhibitory effect on it is the Renshaw inhibitory neuron (Figure). Such a connection in the central nervous system is usually called reverse negative.

3. Lateral inhibition. This is a process in which the excitation of one neural circuit leads to inhibition of a parallel one with the same functions. It is carried out through intercalary neurons.

Inhibition in the nervous system– this is not a passive process of lack of activity, but an active blocking activity. In the case of inhibition, not EPSPs (excitatory), but inhibitory postsynaptic potentials, IPSPs, appear on the membrane. When IPSP occurs, hyperpolarization of the membrane occurs. IPSP causes not a decrease, but an increase in the potential difference across the membrane, which prevents the formation of an action potential. Converging currents are formed on the membrane, that is, hyperpolarization “flows” to the axon from all places where the inhibitory effect occurred. IPSPs arise when anions enter the cell and easily pass through the channels. Most often this is Cl-.

Previously, it was believed that different mediators were responsible for the occurrence of EPSPs and IPSPs. The main inhibitory transmitters include GABA (in the cortical and subcortical regions) and glycine (in the periphery and SC). However, it is now believed that it is not the transmitter itself that is responsible for the generation of EPSPs or IPSPs (GABA can also cause an activating effect). The mediator, entering the postsynaptic membrane, binds to the receptor, which, in turn, affects a special G-protein that activates ion channel proteins. The G protein binds to a messenger intermediary that influences the operation of the ion channel. Depending on the activity of this G protein, either anion or cation channels open, and, accordingly, either an EPSP or an IPSP is generated.

There are pre- and postsynaptic inhibition.

Postsynaptic inhibition

Postsynaptic stimulation reduces the excitability of the cell, making it less sensitive to all excitatory inputs. Postsynaptic inhibition usually develops under the influence of glycine and GABA. Acting on ionotropic receptors, they increase the permeability of the membrane to Cl- (chlorine channels open). Chlorine enters the cell according to concentration gradient, cell hyperpolarization develops, and IPSPs are generated. Inhibition is also possible due to the release of K+ ions from the cell.

Simple forward braking. An inhibitory neuron is inserted into the chain of neurons. The process of inhibition, unlike the process of excitation, does not spread.

Collateral recurrent inhibition. The neuron sends the collateral of its axon to the inhibitory neuron, which, in turn, sends the axon to the first one, inhibiting it. The circle closes, the excitatory cell is inhibited. This mechanism exists in the thalamic system. They are given the rhythm of oscillations (for example, alpha rhythm).

Presynaptic inhibition

The target cell is prevented from generating AP. Presynaptic inhibition causes a decrease in the amount of transmitter released from presynaptic terminals. The difference between presynaptic inhibition and postsynaptic inhibition is that IPSPs are not recorded here, but a decrease in EPSP amplitude occurs.

Braking at axo-axonal synapse. The presynaptic membrane hyperpolarizes and does not release transmitter. Presynaptic inhibition is much more specific and directed to a specific input, giving the cell the opportunity to integrate information from other inputs.

MECHANISMS OF CENTRAL BRAKING.

PRINCIPLES OF COORDINATION ACTIVITY OF THE CNS

Duration of study of the topic_______________ hours

Of these, ___________ hours per lesson; independent work_________ hours.

Location training room

Target: Know the types and mechanisms of central inhibition; Be able to evaluate the role of central inhibition in coordinating the reflex activity of the body.

Tasks:

Know the history of the discovery of central inhibition (Sherrington, Sechenov, Goltz) and modern research that made it possible to reveal its nature (Eccles, Renshaw);

Be able to list the main types of central inhibition, associated and not associated with the function of special inhibitory neurons;

Be able to characterize the essence, mechanism and main types of postsynaptic inhibition;

Know the mediators and ion mechanisms inhibitory potentials (IPSPs), underlying postsynaptic inhibition;

Be able to characterize the essence and mechanism of presynaptic inhibition;

Know the transmitter and ionic IPSPs that underlie presynaptic inhibition;

Be able to characterize the fundamental possibilities of neural activity that contribute to the weakening of the excitation process (inhibition following excitation, pessimum, occlusion);

Be able to clearly define biological significance and the possibility of the occurrence of each type of central inhibition;

Be able to consider the interaction of excitation and inhibition processes as necessary condition for the best implementation of reflex acts of the body;

Know that the coordination of reflexes is based on the principles and features of the spread of excitation and inhibition in the central nervous system;

Know the essence of the most important principles of the coordination activity of the central nervous system (reciprocity, feedback, occlusion, facilitation, final path, dominant, subordination).

The nervous system of humans and animals can be represented as a system of neural chains transmitting excitatory and inhibitory signals (nervous network). These elementary neural circuits serve, for example, to strengthen weak signals, reduce excessive activity, highlight contrasts, maintain rhythms, or maintain the working state of neurons by adjusting their inputs. Such neural circuits are built from standard elements that perform the most frequently repeated operations and can be included in the circuits of a wide variety of neural structures.

There are significant quantitative differences in the neural networks of different types vertebrates and invertebrates. Thus, in humans, the nervous system includes about 10 10 elements, in primitive invertebrates - about 10 4 neurons. However, the structure and functioning of all nervous systems have common features. Found in almost all parts of the central nervous system divergence nerve pathways, convergence nerve pathways and various options braking connections between elements of nerve chains.

Divergence and convergence of pathways . Divergence(divergence) path (Figure 2.A) - occurs as a result of contact of one neuron with many neurons of higher orders. For example, the axon of a sensitive neuron entering the spinal cord is divided into many branches (collaterals), which are directed to different segments of the spinal cord and to the brain, where signal transmission occurs to intercalary and then to motor nerve cells. Divergence of the signal path is also observed in intercalary and effector neurons.

Fig 2. Divergence (A), convergence (B) and spatial summation (C) of nerve pathways in the central nervous system.

The divergence of the path ensures an expansion of the scope of the signal; thanks to it, information arrives simultaneously to different parts of the central nervous system. It's called irradiation excitation (or inhibition). Divergence is so common that we can talk about the principle of divergence in neural circuits.

Convergence- this is the convergence of many nerve pathways to the same neurons (Figure 2.B). For example, in vertebrates, on each motor neuron of the spinal cord and brain stem, thousands of sensory, as well as excitatory and inhibitory interneurons of different levels form nerve endings. Powerful convergence is also found on neurons of the reticular formation of the brainstem, on many cortical neurons in vertebrates, and, apparently, on command neurons.

The convergence of many neural pathways to a single neuron makes that neuron an integrator of relevant signals. The probability of excitation of such an integrator neuron depends not on each incoming stimulus separately, but on the sum and direction of stimuli acting simultaneously, that is, the sum of all synaptic processes occurring on its plasma membrane. In other words, the probability of excitation propagation through the integrator neuron is determined by the algebraic addition of the values of the excitatory and inhibitory inputs on it that are currently active. This addition is the result or spatial or temporal summation. Spatial summation– the result of the addition of nerve impulses arriving simultaneously to a neuron through different synapses (Figure 2.B), time summation– addition of arrivals one by one, through one synapse at short time intervals. In both cases, the integrator neuron is called the common path for nerve signals converging on it, and if we're talking about about a motor neuron, i.e., the final link of the nervous path to the muscles, they talk about common final path.

The result of the summation is the possibility of changing the direction of propagation of excitation in the central nervous system (that is, not strictly within one reflex arc), and therefore changing the nature of the body's response in response to the action of the stimulus. The body's response, realized as a result, becomes more adequate to external conditions and the state of the nervous system. An example of such a choice of answer can be seen if we are talking about convergence not on one neuron, but on a group of neurons jointly regulating a common function, which is not uncommon in the central nervous system. The presence of convergence of multiple paths on one group of motor neurons underlies phenomena spatial relief and occlusion.

Spatial relief- this is the excess of the effect of the simultaneous action of two relatively weak afferent excitatory inputs to the central nervous system over the sum of their separate effects. Those. with separate action of afferent signals, excitation occurs in a smaller number of efferent neurons and the effect is weaker. The phenomenon is explained by the summation of jointly occurring EPSPs to a critical level of depolarization in a group of motor neurons in which, when the inputs were activated separately, the EPSPs turned out to be too weak to generate a response.

Occlusion is a phenomenon opposite to spatial relief. In this case, the effect will be greater if the afferent signals act separately, and when they act together, a smaller group of motor neurons is excited. The reason for occlusion is that here the afferent inputs, due to convergence, are partially connected to the same motor neurons, and each can excite them, as well as both inputs together.

Thus, if the effect of several stimuli delivered simultaneously or in rapid succession is greater than the sum of the effects of the individual stimuli, then this phenomenon is called facilitation; if the effect on a combination of stimuli is less than the sum of responses to individual stimuli, then this phenomenon is occlusion.

This phenomenon should be taken into account, for example, when training various functional indicators of skeletal muscles.

Simple brake and booster chains.

Brake chains, types of braking. Inhibition, like excitation, is an active process; it arises as a result of complex physicochemical changes in tissues. Thanks to the process of inhibition, the spread of excitation in the central nervous system is limited and coordination of reflex acts is ensured; externally, this process is manifested by a weakening of the function of any organ.

The discovery of inhibition in the central nervous system was made by the founder of Russian physiology I.M. Sechenov. In 1862, he conducted classical experiments called “central inhibition.” I.M. Sechenov placed a crystal of sodium chloride (table salt) on the visual tubercles of the frog, separated from the cerebral hemispheres, and observed an increase in the time of spinal reflexes. After the stimulus was removed, the reflex activity of the spinal cord was restored. The results of this experiment allowed I.M. Sechenov to conclude that in the central nervous system, along with the process of excitation, an inhibition process also develops, which can inhibit the reflex acts of the body.

To date, analysis of inhibitory phenomena in the central nervous system has made it possible to distinguish two forms: postsynaptic and presynaptic inhibition.

Postsynaptic inhibition develops on the postsynaptic membranes of interneuron synapses and is associated with hyperpolarization of the postsynaptic membrane under the influence of mediators that are released upon excitation of special inhibitory neurons. At the same time, hyperpolarization that occurs locally on the postsynaptic membrane - inhibitory postsynaptic potential (IPSP) - complicates the electrotonic propagation of excitatory postsynaptic potentials (EPSPs) from other synapses to the axon hillock. As a result, in the area of the axon hillock the membrane potential does not rise to a critical level. An action potential is not formed and the neuron is not excited.

Postsynaptic inhibition is actively used in neural networks, and depending on the options for connecting neurons to each other, several types are distinguished: reciprocal (direct), parallel, reciprocal, lateral (Fig. 3)

Reciprocal inhibition(Figure 3.A) is a mutual (conjugate) inhibition of the centers of antagonistic reflexes, ensuring the coordination of these reflexes. A classic example of reciprocal inhibition is the inhibition of antagonist muscle motoneurons in vertebrates. Inhibition is carried out using special inhibitory interneurons. When the pathways that excite, for example, the motor neurons of the flexor muscles are activated, the motor neurons of the extensor muscles are inhibited by the impulses of the intercalary cells.

Return braking (Fig. 3.B) - This is the inhibition of neurons by their own impulses arriving via return collaterals to the inhibitory cells. Recurrent inhibition is observed, for example, in motor neurons of the spinal cord of vertebrates. These cells send reentrant collaterals into the brain to inhibitory intercalary Renshaw cells, which have synapses on the same motor neurons. Inhibition restricts the rhythm of motor neurons, allowing alternating contraction and relaxation of skeletal muscle, which is important for the normal functioning of the motor system.

The same role is played by recurrent inhibition in other nerve networks.

Parallel braking (Fig. 3.B) – plays a similar role to the recurrent one, but in this case the excitation blocks itself, sending an inhibitory signal to the neuron which simultaneously activates.

This is possible if the excitatory impulse itself should not cause excitation on the target neuron, but its role is important during spatial summation, in combination with other signals.

Lateral inhibition (Fig. 3.D) – This is inhibition of nerve cells located adjacent to the active one, which is initiated by this cell. In this case, a zone appears around the excited neuron in which very deep inhibition develops.

Lateral inhibition is observed, for example, in competing sensory communication channels. It is observed in neighboring elements of the retina of vertebrates, as well as in their visual, auditory and other sensory centers. In all cases, lateral inhibition provides contrast, i.e., isolating significant signals or their boundaries from the background.

Rice. 3. Types of postsynaptic inhibition: A - reciprocal, B - reciprocal, C - parallel, D - lateral. Dark neurons are excitatory, light neurons are inhibitory.

Presynaptic inhibition develops in axo-axonal synapses formed at the presynaptic terminals of the neuron.

Presynaptic inhibition is based on the development of slow and prolonged depolarization of the presynaptic terminal, which leads to the development of inhibition. In the depolarized area, the process of propagation of excitation is disrupted and the impulses arriving at it, not being able to pass through the depolarization zone in the usual quantity and amplitude, do not ensure the release of a sufficient amount of transmitter - the neuron is not excited.

Depolarization of the presynaptic terminal is caused by special inhibitory interneurons, the axons of which form synapses on the presynaptic terminals of the target axon.

The types of presynaptic inhibition have not been sufficiently studied; they are probably the same as for postsynaptic inhibition. The presence of parallel and lateral presynaptic inhibition is precisely known (Fig. 4).

Rice. 4. Types of presynaptic inhibition: A – parallel, B – lateral. Dark neurons are excitatory, light neurons are inhibitory.

In reality, the relationship between excitatory and inhibitory neurons is much more complex than shown in the figures; however, all variants of pre- and postsynaptic inhibition can be combined into two groups. Firstly, when one’s own path is blocked by the spreading excitation itself with the help of intercalary inhibitory cells (parallel and recurrent inhibition), secondly, when other nerve elements are blocked under the influence of impulses from neighboring excitatory neurons with the inclusion of inhibitory cells (lateral and direct inhibition).

In addition, inhibitory cells themselves can be inhibited by other inhibitory neurons, which can facilitate the spread of excitation.

The role of the inhibition process.

Both known types of inhibition, with all their varieties, perform, first of all, a protective role. Lack of inhibition would lead to depletion of transmitters in neuronal axons, fatigue, exhaustion and cessation of central nervous system activity.

Inhibition plays an important role in processing information entering the central nervous system. This role is especially pronounced in presynaptic inhibition.

It regulates the excitation process more precisely, since individual nerve fibers can be completely blocked by this inhibition. Hundreds and thousands of different impulses can arrive at one excitatory neuron along different paths, but the number of impulses reaching the neuron is determined by presynaptic inhibition.

Since blockade of inhibition leads to widespread irradiation of excitation and convulsions, it should be recognized that inhibition is an important factor in ensuring the coordination activity of the central nervous system. Reinforcing circuits and amplification mechanisms

. Neural networks have not only inhibitory mechanisms that prevent the spread of excitation, but also systems that amplify the signal coming to them. Let's look at some of them. WITH self-exciting nerve circuits (circuits with positive feedback) (Fig. 5). Some evidence suggests that in the brains of animals and humans there are closed self-exciting chains of neurons in which neurons are connected by excitatory synapses. Having arisen in response to an external signal, excitation circulates in such a chain, otherwise reverberates

, until either some external brake turns off one of the chain links, or fatigue occurs in it. The output paths from such a chain (branching along the collaterals of the axons of nerve cells that are members of the chain) during operation transmit a uniform flow of impulses, creating one or another setting in the target nerve cells. Its functions may be to ensure long-term maintenance of once induced activity.

Fig.5. Self-exciting neural circuit

Thus, the self-exciting chain, while it is working, seems to “remember” that brief signal that turned on the circulation (reverberation) of pulses in it. It is believed that this is a possible mechanism (or one of the mechanisms) of short-term memory, but there is practically no experimental evidence for this.- an increase in the amplitude of the postsynaptic potential, if the interval between the successive occurrence of action potentials in the presynaptic membrane is small, that is, frequent and rhythmic activation of the synapse occurs. The phenomenon of potentiation is associated with the accumulation of calcium ions in the presynaptic terminal, which is additionally injected there with each new stimulus and does not have time to be completely removed between frequent stimuli. As a result, each new presynaptic potential causes the release of more quanta of the transmitter.

Has the same nature post-tetanic potentiation. In this case, an increase in the number of transmitter quanta released by a nerve impulse after previous rhythmic stimulation leads to an increase in the synaptic response of the neuron to a single stimulation of the presynaptic pathways. Post-tetanic potentiation can last from several minutes to several hours in various brain structures. It is assumed that postsynaptic potentiation plays an important role in plastic rearrangements of synapse functions, and underlies the mechanisms of organization of conditioned reflexes and memory. For example, particularly long-term post-tetanic potentiation has been found in the hippocampus, a structure that appears to play an important role in memory and learning.

Rhythmic stimulation can also lead to a decrease in synaptic activity. The process of reducing postsynaptic potentials during or after the end of tetanic stimulation compared to the initial amplitude is called synaptic depression; By analogy with potentiation, a distinction is made between tetanic and post-tetanic depression. It is possible that synaptic depression occurs in many areas of the nervous system and is a neural correlate of habituation. In invertebrates, the habituation of simple behavioral responses directly corresponds to the depression of the synapses involved; the same applies to the flexor reflex in a cat. Thus, synaptic depression, like synaptic potentiation, constitutes an elementary learning process.

Principles of coordination in the activities of the central nervous system.

Under physiological conditions, the work of all organs and systems of the body is coordinated: the body reacts to influences from the external and internal environment as a single whole. The coordinated manifestation of individual reflexes that ensure the implementation of integral work acts is called coordination.

Coordination phenomena play an important role in the activity of the motor apparatus. Coordination of motor acts such as walking or running is ensured by the interconnected work of nerve centers.

Due to the coordinated work of the nerve centers, the body perfectly adapts to the conditions of existence. This occurs not only due to the activity of the motor system, but also due to changes in the autonomic functions of the body (respiration processes, blood circulation, digestion, metabolism, etc.).

A number of general principles have been established - principles of coordination: the principle of convergence; principle of excitation irradiation; principle of reciprocity; the principle of sequential change of excitation by inhibition and inhibition by excitation; the phenomenon of “recoil”; chain and rhythmic reflexes;

the principle of a common final path; feedback principle; principle of dominance.

Let's look at some of them. The principle of convergence

. This principle was established by the English physiologist Sherrington. Impulses entering the central nervous system through different afferent fibers can converge (converge) to the same intercalary and efferent neurons. The convergence of nerve impulses is explained by the fact that there are several times more afferent neurons than efferent neurons, therefore afferent neurons form numerous synapses on the bodies and dendrites of efferent and interneurons. Irradiation principle

. Impulses entering the central nervous system with strong and prolonged stimulation of the receptors cause excitation not only of this reflex center, but also of other nerve centers. This spread of excitation in the central nervous system is called irradiation. The process of irradiation is associated with the presence in the central nervous system of numerous axonal branches and especially dendrites of nerve cells and chains of interneurons, which connect various nerve centers with each other. The principle of reciprocity

It manifests itself most clearly in animals with a removed brain and a preserved spinal cord (spinal animal), but conjugate, reciprocal inhibition of other reflexes can also occur. Under the influence of the brain, reciprocal relationships can change. A person or animal, if necessary, can bend both limbs, jump, etc.

The reciprocal relationships between the centers of the brain determine a person’s ability to master complex labor processes and no less complex special movements performed during swimming, acrobatic exercises, etc.

The principle of a common final path. This principle is associated with the structural features of the central nervous system. This feature, as already indicated, is that there are several times more afferent neurons than efferent neurons, as a result of which various afferent impulses converge to common outgoing pathways.

The quantitative relationships between neurons can be schematically represented in the form of a funnel: excitation flows into the central nervous system through a wide socket (afferent neurons) and flows out of it through a narrow tube (efferent neurons). Common pathways can include not only terminal efferent neurons, but also intercalary ones.

Impulses converging on a common path “compete” with each other for the use of this path. This achieves ordering of the reflex response, subordination of reflexes and inhibition of less significant ones. At the same time, the body gains the opportunity to respond to various stimuli from the external and internal environment with the help of a relatively small number of executive organs.

Feedback principle. This principle was studied by I.M. Sechenov, Sherrington, P.K. Anokhin and a number of other researchers. During reflex contraction of skeletal muscles, proprioceptors are excited. From proprioceptors, nerve impulses carrying information about the characteristics of this muscle contraction again enter the central nervous system. This controls the accuracy of the movements performed. Similar afferent impulses arising in the body as a result of the reflex activity of organs and tissues (effectors) are called secondary afferent impulses, or feedback.

Feedback can be positive or negative. Positive feedbacks contribute to the strengthening of reflex reactions, negative ones - to their inhibition. Due to positive and negative feedback, for example, regulation of the relative constancy of blood pressure is carried out.

The principle of dominance. The principle of dominance was formulated by A. L. Ukhtomsky. This principle plays an important role in the coordinated work of nerve centers. The dominant is the temporarily dominant focus of excitation in the central nervous system, which determines the nature of the body's response to external and internal stimuli.

The dominant focus of excitation is characterized by the following basic properties:

increased excitability;

persistence of excitement;

ability to sum up excitation;

inertia, the dominant in the form of traces of excitation can persist for a long time even after the cessation of the irritation that caused it.

The dominant focus of excitation is capable of attracting (attracting) nerve impulses from other nerve centers that are less excited at the moment. Due to these impulses, the activity of the dominant increases even more, and the activity of other nerve centers is suppressed.

Dominants can be of exogenous and endogenous origin. Exogenous dominance occurs under the influence of environmental factors. For example, when reading an interesting book, a person may not hear music playing on the radio at that time.

Endogenous dominant occurs under the influence of factors of the internal environment of the body, mainly hormones and other physiologically active substances. For example, when the content of nutrients in the blood, especially glucose, decreases, the food center is excited, which is one of the reasons for the food orientation of the body of animals and humans.

The dominant may be inert (persistent), and for its destruction the emergence of a new, more powerful source of excitation is necessary.

The dominant underlies the coordination activity of the body, ensuring the behavior of humans and animals in the environment, as well as emotional states and attention reactions. The formation of conditioned reflexes and their inhibition is also associated with the presence of a dominant focus of excitation.