Inhibition in the CNS - active nervous process, the result of which is the termination 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 reflex activity spinal cord
BRAKING PROCESSES
IN THE CENTRAL NERVOUS SYSTEM
Along with the mechanisms of excitation in the CNS, there are also mechanisms of inhibition, which manifest themselves in the cessation or decrease in the activity of nerve cells. In contrast to excitation, deceleration is a local non-propagating process that occurs on cell membrane. Sechenov's inhibition. 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. An incision was made in the brain of a frog at the level of the visual tubercles and the time of the withdrawal reflex of the hind paw was measured when it was immersed in a solution of sulfuric acid (Türk's method). When applied to the incision of the visual tubercles of the crystal table salt reflex time
increased. The cessation of the effect of salt on the visual tubercles led to the restoration of the initial time of the reflex reaction. The reflex of the Shdershian paw is due to the excitation of the spinal centers. A salt crystal, irritating the visual tubercles, causes excitation, 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 CNS neurons. In this case, one excitation inevitably becomes inhibitory, and the other - inhibitory. Suppression by one
excitation of another occurs both at the level of postsynaptic membranes
(postsynaptic inhibition), and by reducing the efficiency of excitatory synapses at the presynaptic level (presynaptic inhibition).
presynaptic inhibition. Presynaptic 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, blocking of the conduction occurs.
impulses of excitation along the presynaptic pathways to the hyustsinaitic nerve cell.
postsynaptic inhibition. The most widespread in the CNS is the mechanism of post-synaptic
inhibition, which is carried out by special inhibitory intercalary nerve cells, for example, Renshaw cells in the spinal cord or Purkinje cells (pear-shaped neurons) in the cerebellar cortex]. A feature of inhibitory nerve cells is that their synapses contain mediators that cause TPSP on the postsynaptic membrane of the neuron, i.e. transient hyperpolarization. For example, for motor neurons of the spinal cord, the hyperpolarizing mediator is the amino acid glycine, and for many neurons of the cortex big brain such a mediator is gamma-aminobutyric acid -
GABA. A special case of postsynaptic 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 centers of inhalation and exhalation, the pressor and depressor vasomotor centers are alternately inhibited reciprocally in the medulla oblongata.
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 discriminator ability of the analyzers. Thus, in the auditory analyzer, lateral inhibition provides a distinction between 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 contributes to the differentiation of two points of contact.
The role of inhibition
1) Both types of inhibition with all types of their varieties perform a protective role (the absence would lead to the depletion of mediators in the axons of neurons and the cessation of the activity of the central nervous system);
2) Plays an important role in the processing of information entering the central nervous system;
3) Ensuring the coordination activity of the central nervous system.
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Ticket 15. The 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 cerebral hemispheres from a frog and determined the time of the spinal reflex to irritation of the paw with sulfuric acid. Then to the thalamus, i.e. visual mounds imposed a crystal of table salt and found that the time of the reflex increased significantly. This indicated the inhibition of the reflex. Sechenov concluded that the overlying N.Ts. when Spoi is excited, the underlying ones slow down. Inhibition in the CNS prevents the development of excitation or weakens the ongoing excitation. An example of inhibition may 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 the Dale principle: one neuron - one neurotransmitter. According to it, inhibition is provided by the same neurons and synapses as excitation. Subsequently, the correctness of the binary-chemical theory was proved. In accordance with the latter, inhibition is provided by special inhibitory neurons, which are intercalary. These are Renshaw cells of the spinal cord and neurons of Purkinje intermediate. Inhibition in the CNS is necessary for the integration of neurons into a single nerve center.
Ticket 16. Braking, its types, mechanisms and
functional value.
Braking- an active nervous process caused by excitation and manifested in the suppression or prevention of another wave of excitation. Provides (together with excitation) the normal activity 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 opened in 1863 by I. M. Sechenov.
Primary braking
Primary inhibition occurs in special inhibitory cells adjacent to the inhibitory neuron. At the same time, inhibitory neurons secrete the corresponding neurotransmitters.
Types: 1) Postsynaptic - the main type of primary inhibition, is caused by excitation of Renshaw cells and intercalary neurons. With this type of inhibition, hyperpolarization of the postsynaptic membrane occurs, which causes inhibition.
Examples of Primary Inhibition:
Reverse - the neuron affects the cell, which in response inhibits the same neuron.
Reciprocal - this is mutual inhibition, in which the excitation of one group of nerve cells ensures the inhibition of other cells through the intercalary neuron.
Lateral - inhibitory cell inhibits nearby neurons. Similar phenomena develop between the bipolar and ganglion cells of the retina, which creates conditions for a clearer vision of the object.
Reverse facilitation - neutralization of neuron inhibition during inhibition of inhibitory cells by other inhibitory cells.
Presynaptic - occurs in ordinary neurons, 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 a secondary inhibition that develops in excitatory synapses as a result of a 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 process of excitation. 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 the membrane depolarization to a critical level of depolarization; voltage-gated sodium channels do not open and an action potential does not arise.
Peripheral inhibition- Conditional and unconditional braking
The terms "conditional" and "unconditional" inhibition were proposed by I. P. Pavlov.
Conditioned, or internal, inhibition is a form of inhibition of a conditioned reflex that occurs when conditioned stimuli are not reinforced by unconditioned ones. Conditioned inhibition is an acquired property and is developed in the process of ontogeny.
Classification of types of central inhibition. Primary and Secondary
Conditioned inhibition is central inhibition and weakens with age.
Unconditional (external) braking- inhibition of the conditioned reflex, which occurs under the influence of unconditioned reflexes(for example, the orienting reflex). IP Pavlov attributed unconditioned inhibition to the innate properties of the nervous system, that is, unconditioned inhibition is a form of central inhibition.
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Inhibition in the CNS (I.M. Sechenov). presynaptic and postsynaptic inhibition. Inhibitory neurons and mediators. Significance of inhibition in nervous activity. C21-22
Methods of physiological research (observation, acute experience and chronic experiment). The contribution of domestic and foreign physiologists to the development of physiology. C 1-2
Communication of physiology with disciplines: chemistry, biochemistry, morphology, psychology, pedagogy and theory and methodology of physical education. C3
The main 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 arousal. C 4-6
excitability parameters. Threshold of the strength of irritation (rheobase). Chronaxia. Change in excitability during excitation, 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 the reflex arc, reflex time. C 9-11
Nervous and humoral mechanisms of regulation of functions in the body and their interaction. C 11-13
Neuron: structure, functions and classification of neurons. Features of the conduction of nerve impulses along axons. C 13-14
synapse structure. mediators. Synaptic transmission of a nerve impulse. 15-17
The concept of the nerve center. Features of the conduction of excitation through the nerve centers (one-sided conduction, delayed conduction, summation of excitation, transformation and assimilation of the rhythm). C 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. C 18-21
Inhibition in the CNS (I.M. Sechenov). presynaptic and postsynaptic inhibition. Inhibitory neurons and mediators. Significance of inhibition in nervous activity. C21-22
15. General plan of the structure and function of sensory systems. The mechanism of excitation of receptors (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 (IPSP) or depolarization of the presynaptic nerve ending with which another nerve ending of the axon.
Therefore, central (primary) postsynaptic inhibition and central (primary) presynaptic inhibition are distinguished.
Post-synaptic inhibition (Latin post behind, after something + Greek sinapsis contact, connection) is a nervous process caused by the action on the postsynaptic membrane of specific inhibitory mediators (glycine, gamma-aminobutyric acid) secreted by specialized presynaptic nerve endings. The mediator secreted by them changes the properties of the postsynaptic membrane, which causes suppression of the cell's ability to generate excitation. In this case, a short-term increase in the permeability of the postsynaptic membrane to K+ or CI- ions occurs, causing a decrease in its input electrical resistance and generation of inhibitory postsynaptic potential (IPSP). The occurrence of IPSP in response to afferent stimulation is necessarily associated with the inclusion in the inhibitory process of an additional link - an inhibitory interneuron, the axonal endings of which release an inhibitory neurotransmitter.
Presynaptic inhibition (Latin prae - ahead of something + Greek sunapsis contact, connection) is a special case of synaptic inhibitory processes that manifest themselves 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 mediator release by excitatory nerve endings . In this case, the properties of the postsynaptic membrane do not undergo any changes. Presynaptic inhibition is carried out by means of special inhibitory interneurons. Its structural basis is axo-axonal synapses formed by axon terminals of inhibitory interneurons and axonal endings of excitatory neurons.
In this case, the axon ending of the inhibitory neuron is presympathetic with respect to the terminal of the excitatory neuron, which is postsynaptic with respect to the inhibitory ending and presynaptic with respect to the nerve cell activated by it. In the endings of the presynaptic inhibitory axon, a mediator is released, which causes depolarization of excitatory endings by increasing the permeability of their membrane for CI-. Depolarization causes a decrease in the amplitude of the action potential arriving at the excitatory ending of the axon. As a result, the mediator release process is inhibited by excitatory nerve endings and the amplitude of the excitatory postsynaptic potential decreases.
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 passes stronger ones, therefore, it serves as a mechanism for isolating, isolating more intense afferent impulses from the general flow. This is of great adaptive importance for the organism, since of all the afferent signals going to the nerve centers, the most important, the most necessary for a given specific time, stand out. Thanks to this, the nerve centers, the nervous system as a whole, are freed from the processing of less essential information.
29. Secondary braking. His types. Origin mechanism. Principles of CNS coordination activity (convergence, common end point, divergence, irradiation, reciprocity, dominant).
Secondary. It does not require special inhibitory structures, it arises as a result of a change in the functional activity of ordinary excitable structures, it is always associated with the process of excitation. Types of secondary braking:
a) beyond, arising from a large flow of information entering the cell. The flow of information lies outside the neuron's working capacity; b) pessimal, arising at a high frequency of stimulation;
c) parabiotic, arising from strong and long-acting 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, protects the central neurons from overexcitation. Inhibition in the central nervous system can occur when nerve impulses of various strengths from several stimuli simultaneously enter the spinal cord. Stronger stimulation inhibits the reflexes that should have come in response to weaker ones.
Coordination activity (CA) of the CNS is a coordinated work of CNS neurons based on the interaction of neurons with each other.
CD functions:
1) provides a clear performance of certain functions, reflexes; 2) ensures the consistent inclusion of various nerve centers in the work to ensure complex forms of activity; .
Basic principles of CNS CD and their neural mechanisms.
1. The principle of irradiation (spread). 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 can 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 at the moment. This is a focus of persistent, unwavering, non-spreading excitation.
According to IP Pavlov's definition, excitation and inhibition are two sides of the same process. The coordination activity of the CNS provides a clear interaction between individual nerve cells and individual groups of nerve cells. There are three levels of integration.
The first level is provided due to the fact that impulses from different neurons can converge on the body of one neuron, as a result, either summation or a decrease in excitation occurs.
The second level provides interactions between separate groups of cells.
The third level is provided by the cells of the cerebral cortex, which contribute to a more perfect 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 the transverse section of the visual tubercles of a frog or an electrical weak current is applied, then the time of the Türk reflex is sharply extended (the Türk reflex is the bending of the paw when it is immersed u into acid). Soon new facts were discovered demonstrating the phenomena of inhibition in the central nervous system. Goltz showed that the Turk reflex is inhibited by squeezing the other paw with tweezers, Sherrington proved the presence of inhibition of the reflex contraction of the extensor during the flexion reflex. It was proved that in this case the intensity of reflex inhibition depends on the ratio of the strength of the excitatory and inhibitory stimuli.
In the central nervous system There are several ways of braking, which have a different nature and different localization. but in principle based on the same mechanism - an increase in the difference between the critical level of depolarization and the magnitude of the membrane potential of neurons.
1. postsynaptic inhibition. inhibitory neurons . It has now been established that in the CNS, along with excitatory neurons, there are special inhibitory neurons. An example is the so-called. Renshaw cell in the spinal cord. Renshaw discovered that the axons of motor neurons, before exiting the spinal cord, give rise to one or more collaterals that terminate on special cells whose axons form inhibitory synapses on the motor neurons of this segment. Due to this, the excitation that occurs in the motor neuron propagates along the direct path to the periphery to the skeletal muscle, and activates the inhibitory cell along the collateral, which suppresses further excitation of the motor neuron. This is a mechanism that automatically protects nerve cells from excessive excitation. Inhibition, carried out with the participation of Renshaw cells, is called recurrent postsynaptic inhibition. The inhibitory mediator in Renshaw cells is glycine.
Nerve impulses arising from the excitation of inhibitory neurons 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 mediator is released that 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 thus prevents the achievement of the critical level of membrane depolarization necessary for the occurrence of propagating excitation. Postsynaptic inhibition can be eliminated by strychnine, which blocks inhibitory synapses.
2.Posttetanic inhibition. A special type of inhibition is one that 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 the critical depolarization of the membrane and the generation of propagating excitation. The reason for this inhibition is that trace potentials are capable of summation, and after a series of frequent pulses, 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 a strong depolarization of the postsynaptic membrane under the influence of too frequent impulses (as a pessimum in a neuromuscular preparation).
Intermediate neurons of the spinal cord, neurons reticular formation. With persistent depolarization, a state similar to Verigo's cathodic depression sets in.
4.presynaptic inhibition. It was discovered relatively recently in the CNS, therefore, it has been studied less. Presynaptic inhibition is localized in the presynaptic terminals in front of the synaptic plaque. The axon endings of other nerve cells are located on the presynaptic terminals, forming axo-axonal synapses here. Their mediators depolarize the membrane of the terminals and bring them into a state similar to Verigo's cathodic depression. This causes a partial or complete blockade of the conduction of excitatory impulses along the nerve fibers going to the nerve endings. Presynaptic inhibition is usually prolonged.
Braking classification-
1. Primary inhibition - specialized inhibitory neurons with special mediators (GABA, glycine) a- postsynaptic b-presynaptic
2. Secondary inhibition - in excitatory synapses in a certain state a) pessimal b) after excitation
Inhibition in the CNS. inhibitory neurons. inhibitory synapses. The mechanism of occurrence of inhibitory postsynaptic potential (IPSP). Inhibitory mediators, their receptors. Interaction of EPSP and IPSP on a neuron. The role of inhibition in the CNS.
Integrative and coordinating activities of central nerve formations carried out with the mandatory participation of inhibitory processes.
Inhibition in the central nervous system is an active process that manifests itself externally in the suppression or weakening of the excitation process and is characterized by a certain intensity and duration.
Normal inhibition is 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 nervous structures. The formative effect of the inhibitory process develops in space and time. Inhibition is an innate process, constantly improving during the individual life of the organism.
With a significant strength of the factor that caused inhibition, it can spread over a considerable area, involving large populations of nerve cells in the inhibitory process.
The history of the development of the theory 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 tubercles 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 the logical necessity to explain the complex forms of the coordination activity of the central nervous formations. Subsequently, this assumption found direct experimental confirmation (Eccles, Renshaw), when the existence of special intercalary neurons with synaptic contacts with motor neurons was shown. Activation of these interneurons naturally led to inhibition of motor neurons. Depending on the neural mechanism, the method of inducing an 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 axon processes of which the inhibitory mediator is released and enters the synaptic cleft. The inhibitory effect of such neurons is due to the specific nature of the mediator - a chemical signal carrier from one cell to another. The most common inhibitory neurotransmitter is gamma-aminobutyric acid (GABA). The chemical action of GABA induces the effect of hyperpolarization in the postsynaptic membrane in the form of inhibitory postsynaptic potentials (IPSPs), the spatiotemporal summation of which increases the level of the membrane potential (hyperpolarization), leads to a slowdown or complete cessation of the generation of propagating APs.
Reverse braking called inhibition (suppression) of neuron activity, caused by the recurrent collateral of the axon of the nerve cell. So, the motor neuron of the anterior horn of the spinal cord, before leaving the spinal cord, gives a lateral (recurrent) branch, which returns back and ends on inhibitory neurons (Renshaw cells). The last axon 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 the nerve circuit, which consists of three series-connected neurons (Fig.). The neurons of complex nerve centers have numerous connections with each other, forming three types of nerve networks:
1. Hierarchical. If the excitation spreads to an increasing number of 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, nerve endings from several afferent neurons can approach one motor neuron. In such networks, upstream neurons control downstream ones.
2. Local networks. Contain neurons with short axons. Οʜᴎ provide communication between neurons of one level of the CNS and short-term storage of information at this level. An example of them is a ring chain (rice). In such circuits, excitation circulates for a certain time. Such circulation is usually called reverberation of excitation (mech. short-term memory).
3. Divergent networks with one input. They have one neuron, ᴛ.ᴇ. the input forms a large number of connections with the 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 distribution to all neurons.
As a result of irradiation, excitation can pass to other nerve centers and even cover the entire nervous system.
Nerve networks contain a large number of intercalary neurons, some of which are inhibitory. For this reason, several types of inhibitory processes can 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 inhibition is also called conjugate (Fig).
2. Reverse braking. In this case, the excitation goes from the neuron along the axon to another cell. But simultaneously along the collaterals (branches) to the inhibitory neuron, which forms a synapse on the body of the same neuron. A special case of such braking is Renshaw braking. When the motor neurons of the spinal cord are excited, nerve impulses go along their axons to muscle fibers, but at the same time they propagate along the collaterals of this axon to Renshaw cells. The axons of Renshaw cells form inhibitory synapses on the bodies of the same motor neurons. As a result, the stronger the motor neuron is excited, the stronger the inhibitory effect on it is the Renshaw inhibitory neuron (Fig. Such a relationship in the central nervous system is usually called a negative feedback.
3. Lateral inhibition. This is a process in which the excitation of one neural circuit leads to the inhibition of a parallel one with the same functions. Carried out through intercalary neurons.
Choose one correct answer.
212. EVERYTHING IS REQUIRED FOR THE DEVELOPMENT OF INHIBITION IN THE CNS, EXCEPT
1) mediator
2) ATP energy
3) opening of chloride channels
4) opening of potassium channels
5) violations of the integrity of the nerve center
213. THE MEDIATOR OF THE INDUSTRIAL NEURON, AS A RULE, ON THE POSTSYNAPTIC MEMBRANE, CAUSES
1) static polarization
2) depolarization
3) hyperpolarization
214. REFLEX TIME IN SECHENOV'S EXPERIENCE
1) does not change
2) is not determined in this experiment
3) decreases
4) increases
215. IN SECHENOV'S EXPERIENCE
1) thoracic and lumbar spinal cord
2) medulla oblongata and spinal cord
3) between visual tubercles and overlying departments
216. INHIBITION WAS DISCOVERED BY SECCHENOV AT IRRITATION
1) spinal cord
2) medulla oblongata
3) cerebral cortex
4) cerebellum
5) thalamus
217. DURING THE DEVELOPMENT OF PESSIMAL INHIBITION, THE NEURON MEMBRANE IS IN THE STATE
1) static polarization
2) hyperpolarization
3) sustained prolonged depolarization
218. THE PHENOMENON IN WHICH EXCITATION OF ONE MUSCLE IS ACCOMPANIED BY INHIBITION OF THE CENTER OF THE ANTAGONIST MUSCLE IS CALLED
1) negative induction
2) occlusion
3) relief
4) fatigue
5) reciprocal inhibition
219. BRAKING IS A PROCESS
1) always spreading
2) propagating if IPSP reaches a critical level
3) local
220. SPECIFIC BRAKE NEURONS ARE
1) neurons of the substantia nigra and the red nucleus of the midbrain
2) pyramidal cells of the cerebral cortex
3) neurons of the Deiters nucleus of the medulla oblongata
4) Purkinje and Renshaw cells
221. THE PHENOMENON OF CONNECTED DECELERATION CAN BE OBSERVED
1) in Sechenov's experiment
2) with simultaneous stimulation of the receptive fields of two spinal reflexes
3) in an experiment when, during the development of one reflex, the receptive field of an antagonistic reflex is irritated
222. THE SIGNIFICANCE OF RECIPROCAL INHIBITION IS
1) in the performance of a protective function
2) in the release of the central nervous system from the processing of non-essential information
3) in ensuring the coordination of the work of antagonist centers
223. IPSP DUE TO CHANGES IN THE PERMEABILITY OF THE MEMBRANE FOR IONS
2) sodium and chlorine
3) potassium and chlorine
224. THE APPEARANCE OF PESSIMAL BRAKING IS PROBABLY
1) at low pulse frequency
2) with the secretion of inhibitory mediators
3) upon excitation of intercalary inhibitory neurons
4) with increasing pulse frequency
225. PRESYNAPTIC INHIBITION IS IMPLEMENTED THROUGH SYNAPSES
1) axo-somatic
2) somato-somatic
3) axo-dendritic
4) axo-axonal
226. THE MECHANISM OF PRESYNAPTIC INHIBITION IS RELATED
1) with hyperpolarization
2) with the operation of the K - Na pump
3) with CA pump operation
4) with prolonged depolarization
227. FROM THE POINT OF VIEW OF THE BINARY-CHEMICAL THEORY, THE PROCESS OF BRAKING ARISES
3) in the same structures and with the help of the same mediators as the excitation process
4) during the functioning of special inhibitory neurons that produce special mediators
228. FROM THE POINT OF VIEW OF THE UNITARY-CHEMICAL THEORY, BRAKING APPEARS
1) due to inactivation of cholinesterase
2) with a decrease in the synthesis of the excitatory mediator
3) during the functioning of special inhibitory neurons that produce special mediators
4) in the same structures and with the help of the same mediators as the excitation process
229. THE PHENOMENON OF PESSIMAL BRAKING WAS DISCOVERED
1) Ch. Sherrington
2) I.M. Sechenov
3) I.P. Pavlov
4) the Weber brothers
5) NOT. Vvedensky
230. THE PHENOMENON OF CENTRAL BRAKING WAS DISCOVERED
1) the Weber brothers
2) Ch. Sherrington
3) I.P. Pavlov
4) I.M. Sechenov
231. BRAKING IS A PROCESS
1) arising from the fatigue of nerve cells
2) leading to a decrease in the KUD of the nerve cell
3) arising in receptors with excessively strong stimuli
4) preventing the occurrence of excitation or weakening the excitation that has already occurred
232. BRAKING IS REQUIRED IN THE WORK OF THE NERVE CENTERS
1) to close the arc of reflexes in response to irritation
2) to protect neurons from excessive excitation
3) to combine CNS cells into nerve centers
4) to ensure the safety, regulation and coordination of functions
233. DIFFUSIVE IRRADIATION CAN BE STOP AS A RESULT OF
1) the introduction of strychnine
2) increase the strength of the stimulus
3) lateral inhibition
234. THE DEVELOPMENT OF INDERATION IN SECHENOV'S EXPERIMENT ON A FROG IS JUDGED BY
1) the appearance of convulsive contractions of the legs
2) decrease in heart rate followed by cardiac arrest
3) time change spinal reflex
235. CONTRACTION OF THE FLEXOR MUSCLES WITH SIMULTANEOUS RELAXATION OF THE EXTENSOR MUSCLES IS POSSIBLE AS A RESULT OF
1) outdoor activities
2) relief
3) negative induction
4) pessimal inhibition
5) reciprocal inhibition
236. INHIBITION OF NEURONS BY OWN IMPULSES COMING THROUGH AXON COLLATERALS
TO THE BRAKE CELLS, REFERRED
1) secondary
2) reciprocal
3) progressive
4) lateral
5) returnable
237. WITH THE HELP OF RENSHOW'S BRAKING INTERCHANGE CELLS BRAKING IS CARRIED OUT
1) reciprocal
2) lateral
3) primary
4) returnable
238. INHIBITION OF MOTONEURONS OF ANTAGONIST MUSCLES DURING LIMB FLEXION AND EXTENSION IS CALLED
1) progressive
2) lateral
3) returnable
4) reciprocal
239. WHEN THE LIMB IS BENDED, THE INTERCUTIVE BRAKING NEURONS OF THE CENTER OF THE EXTENSION MUSCLES SHOULD BE
1) at rest
2) are inhibited
3) excited
240. BRAKING EFFECT OF A SYNAPSE LOCATED NEAR THE AXON COLLECTION
COMPARED WITH OTHER PARTS OF THE NEURON MORE
2) strong
241. DEVELOPMENT OF INHIBITION OF NEURONS PROMOTES
1) depolarization of the membrane of the axon hillock and the initial segment
2) depolarization of the soma and dendrites
3) hyperpolarization of the axon colliculus membrane
242. BY ITS MECHANISM, POSTSYNAPTIC INHIBITION CAN BE
1) only depolarizing
3) and de- and hyperpolarizing
243. BY ITS MECHANISM, PRESYNAPTIC INHIBITION CAN BE
1) both de- and hyperpolarization
2) only hyperpolarization
3) only depolarizing
Set a match.
DURING BRAKING..... ON THE SUBSYNAPTIC MEMBRANE
A.2 Presynaptic 1. Short-term depolarization.
B.3 Postsynaptic 2. Prolonged depolarization.
3. Hyperpolarization or prolonged depolarization.
THEORIES OF BRAKING .... ARE THAT
A.3 Unitary-chemical 1. Braking is a consequence of fatigue.
B.2 Binary-chemical 2. Inhibition occurs as a result of the functioning of inhibitory neurons.
3. Inhibition manifests itself in the same structures and with the help of the same mediators as excitation.
NERVOUS PROCESS .... CHARACTERIZE SIGNS
A.2 Excitation 1. Always a local process that manifests itself
B.1 Inhibition in long-term stable depolarization or hyperpolarization of the neuron membrane.
2. Local or spreading process due to the opening of sodium channels.
PHENOMENON.... DEVELOPING AS A RESULT OF
A.4 Pessimal 1. Continuous DC
deceleration in the area of application of the cathode.
B.1 Cathodic 2. Short-term action of direct current in the area of application of the cathode.
depression 3. Irritation of the vagus nerve.
4. Increasing the frequency of impulses.
5. Simultaneous stimulation of the receptive fields of two spinal reflexes.
RESEARCHERS .... CNS PHYSIOLOGY MADE THE FOLLOWING CONTRIBUTION TO THE DEVELOPMENT
A.2 A.A. Ukhtomsky 1. Formulated the principles of general
B.3 Berger of the final path and reciprocity.
B.1 Ch. Sherrington 2. Developed the doctrine of the dominant.
3. First recorded EEG in humans.
BRAKING .... REACTION
A.2 Is 1. Disappearance of the knee jerk in case of trauma to the lumbar spine.
B.1 Is not 2. Cessation of salivation in the process of eating when there is severe pain in the abdomen.
TYPE OF BRAKING....PERFORMS A FUNCTION
A.2 Lateral 1. Suppresses the excitation of the center
B.4 Recurrent antagonistic function.
B.1 Reciprocal 2. Eliminates diffuse irradiation of excitation.
3. Stops the release of the mediator into the synaptic cleft.
4. Weakens the excitation of motor neurons by their own impulses through Renshaw cells.
TYPES OF NEURONS ... ARE
A.3 Alpha motor neuron 1. Neuron of the motor zone of the cerebral cortex.
B.2 Gamma motor neuron 2. Neuron of the anterior horns of the spinal cord,
B.1 Giant pyra - midal skeletal muscle cell innervating intrafusal fibers.
Betsa 3. Neuron of the anterior horns of the spinal cord,
D.5 Renshaw cell innervating extrafusal fibers of skeletal muscles.
4. Inhibitory neuron of the cerebellar cortex.
5. Inhibitory interneuron of the spinal cord.
TYPES OF POSTSYNAPTIC POTENTIALS OF A NEURON ..... ARE DUE TO THE OPENING OF CHANNELS FOR IONS
A.1 EPSP 1. Sodium.
B.23 TPSP 2. Potassium.
4. Calcium.
AT ACTIVATION OF CHLORINE CHANNELS... THE CURRENT OF CHLORINE IONS IS OBSERVED...
A.1 Presynaptic 1. Out of the cell.
B.2 Postsynaptic 2. From the external environment into the cell.
Determine whether the statements are true or false and the relationship between them.
254. Inhibition of the spinal reflex in the experiment of Sechenov is caused by irritation of the visual tubercles with a crystal of sodium chloride, because sodium and chloride ions cause hyperpolarization of neurons.
5) VNN
255. Presynaptic inhibition is very effective in processing information coming to the neuron, because during presynaptic inhibition, excitation can be selectively suppressed at one synaptic input without affecting other synaptic inputs.
5) VVV
256. To demonstrate the role of inhibition, strychnine is injected into a frog, because strychnine activates inhibitory synapses.
5) VNN
257. To demonstrate the role of inhibition, strychnine is injected into a frog, because strychnine blocks inhibitory synapses.
5) VVV
258. To demonstrate the role of inhibition, strychnine is injected into a frog, because after the administration of strychnine, the frog exhibits
diffuse irradiation of excitation.
5) VVV
259. A neuron can be in a state of rest, excitation or inhibition, because on one neuron they can be summed up
either excitatory or inhibitory postsynaptic potentials.
5) VNN
260. Only EPSP or only TPSP can be summed on one neuron, because according to the Dale principle, one neuron uses
in all their terminals there is only one type of mediator.
5) NVN
261. Either excitation or inhibition can spread along the axon of a neuron, because during the summation of EPSP
and IPSP total potential can be either positive or negative.
5) NVN
262. Sechenov's experiment is carried out on a spinal frog, because the time of the spinal reflex is measured in Sechenov's experiment.
5) NVN
263. Sechenov's experiment is carried out on a thalamic frog, because for the manifestation of the spinal reflex in Sechenov's experiment, it is necessary to place a salt crystal on the visual tubercles.
5) VNN
Similar information.
IM Sechenov (1862) discovered inhibition in the central nervous system. He showed that when the area of the visual halls of the frog is stimulated, the motor spinal reflexes are inhibited, since their latent period is very significantly increased. The phenomenon of central inhibition was also confirmed by the students of I. M. Sechenov in animals with a constant body (L. N. Simonov, 1866). The brain not only inhibits spinal reflexes, but under certain conditions enhances them (I. G. Berezin, 1866, V. V. Pashutin, 1866).
Significance of the discovery of central inhibition for the further development of physiology
I. M. Sechenov was the first to prove the influence of the reticular formation of the brain stem on the spinal cord. The discovery of I. M. Sechenov was the starting point for the work of the school of I. P. Pavlov on the study of the patterns of the relationship between excitation and inhibition in the brain and the work of the school of N. E. Vvedensky on the study of the nature of inhibition and the unity of excitation and inhibition.
In all types of central inhibition, caused by impulses coming through afferent fibers, and carried out by efferent impulses along the pyramidal pathways, intercalary ones are involved. A distinction is made between primary inhibition caused by the activation of inhibitory synapses and occurring without prior excitation, and secondary inhibition as a result of previous excitation.
Primary inhibition includes postsynaptic, including recurrent inhibition of motor neurons by Renshaw cells, and presynaptic. Secondary inhibition includes induction inhibition after excitation with reciprocal innervation and pessimal inhibition by N. E. Vvedensky, which is not found in the central nervous system in the norm.
1. Postsynaptic inhibition, in which inhibitory postsynaptic potentials (IPSPs) arise in type 2 inhibitory synapses. In the spinal cord, IPSPs appear in motor neurons and Renshaw neurons under certain conditions of influx of afferent impulses; in the brain, they appear in basket and other inhibitory neurons. In the spinal cord, the latent period of IPSP is 0.3 ms, they reach a maximum after 0.8 ms and last about 2.5 ms. In the neurons of the brain, they last much longer, 100-200 ms. TPSP discharge frequency up to 1000 imp/s. They are also summed up in space and time, as well as EPSP TPSP - almost a mirror image of EPSP (TPSP counteracts EPSP, prevents the resulting depolarization, since hyperpolarization of the postsynaptic membrane occurs during IPSP. When irritation of the afferent nerve, causing inhibition and the appearance of EPSP, precedes EPSP, then the latter is suppressed. Under the action of an inhibitory stimulus during the conduction of EPSP impulses, they become less frequent or disappear. The result of inhibition depends on the ratio of the amplitudes of EPSP and IPSP and the number of participating excitatory and inhibitory synapses.
In mammals, hyperpolarization of the postsynaptic membrane during IPSP exceeds the resting potential by 5-10 mV, and in amphibians by 10-20 mV. Hyperpolarization of the membrane is caused by an inhibitory mediator, which increases its electrical conductivity by almost 10 times. During inhibition, Na ions do not pass through the membrane, they do not participate in the appearance of IPSP, which is caused by a sharp increase in the permeability of the membrane in special inhibitory zones for Cl and K ions. Under the action of an inhibitory mediator, tiny pores are formed in the inhibitory zones of the membrane, passing only small hydrated Cl ions and impervious to large ions. Cl ions move inside the cell according to the electrochemical gradient, their concentration inside the cell increases ("chlorine pump"), which causes hyperpolarization. The output of K ions to the outside according to the electrochemical gradient has less value for the occurrence of hyperpolarization, since it can achieve an increase in only no more than half of the permeability to Cl ions. An increase in the concentration of Cl inside the cell, causing hyperpolarization, can, upon reaching a critical level, cause the reverse movement of these ions, which will lead to depolarization.
Acetylcholine, released in inhibitory synapses upon receipt of impulses through the vagus nerves, inhibits the activity of the vertebrate heart. The impulses coming through the vagus nerves hyperpolarize. Inhibition of heart contractions is due to a sharp increase in the permeability of the myocardial membrane for K ions. In the venous sinus of the frog, acetylcholine also causes an increase in the permeability of the membrane for K ions, and the permeability for Cl ions changes slightly. An increase in the permeability of the membrane for K ions explains the increase in its electrical conductivity. Acetylcholine is an inhibitory neurotransmitter for many synapses.
Norepinephrine is an inhibitory mediator for many smooth muscles and sympathetic ganglion neurons. Irritation of the nerve plexuses in the wall of the alimentary canal causes hyperpolarizing IPSP and inhibits spontaneous contractions of smooth muscles.
Inhibition of synapses is caused by y-aminobutyric acid, which is formed from glutamic acid in the brain. In its chemical composition, it is close to a special inhibitory mediator that causes hyperpolarization of postsynaptic membranes. γ-aminobutyric acid inhibits the conduction of nerve impulses, directly acting on neurons without causing hyperpolarization. However, its mechanism of action differs from that of acetylcholine. This acid is synthesized with the participation of vitamin B 6 .
In crustaceans, inhibitory nerve impulses and γ-aminobutyric acid increase the permeability of the postsynaptic membrane to Cl ions. Their axon is a thousand times less sensitive to this acid than the bodies of neurons and the bases of dendrites, where inhibitory synapses are located.
In the central nervous system and the digestive canal, a protein substance P (polypeptide) was also found, which, possibly, is a mediator. It has a calming effect.
2. Presynaptic inhibition that occurs in the finest branches (terminals) of afferent nerve fibers before they pass to the nerve ending.
These terminals terminate the fibers of inhibitory neurons that form inhibitory synapses.
Presynaptic inhibition involves at least two intercalary inhibitory neurons, so it is longer and more effective than postsynaptic.
During presynaptic inhibition, the permeability of the postsynaptic membrane does not change and, consequently, the excitability of motor neurons does not change. A decrease in EPSP and inhibition of reflex discharges in motor neurons depends on a decrease in excitation impulses coming to them through afferent fibers from muscle receptors. This occurs as a result of primary afferent depolarization (PAD) of the afferent terminals at which the synapses of inhibitory interneurons terminate, in contrast to Renshaw neurons, whose synapses terminate at the body of the motor neuron. PAD is caused by the prolonged action of a mediator that is different from the mediator of postsynaptic inhibition. The neurotransmitter formed in the synapses of inhibitory neurons depolarizes the axon membrane and induces in it a state similar to Verigo's catholic depression. Depolarization of afferent terminals inhibits the release of a mediator that causes EPSP in excitatory synapses of motor neurons. Depolarization of presynaptic fibers inhibits the transmission of impulses from them to motor neurons. Presynaptic inhibition is widespread in the central nervous system of mammals, for example, in the cerebral cortex it prevails over postsynaptic inhibition in most excitatory neurons of the primary afferent fibers. Presynaptic inhibition plays the role of a negative feedback that acts on the influx of sensitive afferent impulses into the central nervous system.
3. Pessimal inhibition by N. E. Vvedensky, which occurs in intercalary neurons and in the reticular formation.
It is likely that the decrease in the EPSP amplitude with excessively frequent rhythmic stimuli (frequency pessimum) is caused by a decrease in the amplitude of the biopotentials entering the presynaptic endings, since even a relatively very small presynaptic depolarization sharply reduces the release of the mediator in excitatory synapses, and hence the amplitude of the EPSP.
4. Inhibition after excitation, which appears with a strong trace hyperpolarization of the neuron membrane.
THEM. Sechenov wrote: “Inhibition of reflexes during stimulation of the visual chambers corresponds to the excited state of the mechanisms contained in them ... These mechanisms, in other words, delay reflexes. The pathways for the distribution of this type of inhibition of reflexes along the spinal cord lie in the anterior parts of the latter.
It should be noted an important circumstance of I.M. Sechenov, namely: reflexes used by I.M. Sechenov in experience, were nociceptive.
According to Sechenov, inhibition of reflex activity necessarily occurs after preliminary excitation of some mechanisms in the visual chambers to which salt is applied, and, therefore, only this primary excitation leads to the final inhibitory effect in the form of a cessation of activity, expressed in the cessation of movements in response to nociceptive irritation of the lower extremities. According to modern ideas, I.M. Sechenov studied inhibition in frogs caused by stimulation of the reticular formation of the brainstem.
THEM. Sechenov objected to understanding inhibition in the central nervous system as fatigue due to overexcitation of nervous structures. He wrote: “Inhibition of reflexes is a product of excitation, and not overexcitation of any nervous mechanisms. This is proved by the fact that the effect develops in the first moments after the application of stimulation, before movements appear. In addition, from the cuts of the visual halls, irritation always gives, next to the inhibition of reflexes, diastolic arrest of the blood heart, that is, it clearly excites the medulla oblongata.
The results of I.M. Sechenov and our studies of some effector manifestations of the action of ketamine indicate the commonality of the physiological mechanisms leading to inhibition of reflex activity during stimulation of the "visual chambers" in the frog and during anesthesia with ketamine.
Indeed, the analysis of electroencephalograms revealed an active, active state of the brain characteristic of ketamine, which, according to modern concepts, is associated with an excited state of the reticular formation of the brain stem, which corresponds to the excitation of the same structures by salt in the experiments of I.M. Sechenov.
Irritation (excitation) of the visual tubercles of a frog according to the method of I.M. Sechenov leads to excitation of the motor neurons of the extensor muscles of the lower extremities - and, consequently, an increase in the amplitude of the monosynaptic reflex - which causes a tonic contraction of the extensor muscles with simultaneous inhibition of flexion reflexes to nociceptive stimulation. An increase in the excitability of the spinal motor neurons of the extensor muscles, revealed by an increase in the amplitude of the Hoffmann reflex with simultaneous inhibition of reflexes to nociceptive stimulation, was also found during anesthesia with ketamine.
On the localization of the inhibition process itself in the system of the integral reflex apparatus I.M. Sechenov wrote: “In relation to the whole problem of delaying reflected movements ... it is by no means possible to look for the basis of the inhibition of reflexes, which occurs as a result of brain irritation, in changes in the motor apparatus ... the delay of reflected movements is carried out in the central formations of the reflex apparatus.”
The results of our study of the excitability of spinal motor neurons during anesthesia with ketamine (the H-reflex method) showed that, in contrast to a significant increase in the amplitude of the reflex H-response, the magnitude of the direct (peripheral) M-response did not change. This gives reason to believe that the noted changes in H- and M-responses during ketamine anesthesia are not associated with the action of ketamine directly in the neuromuscular synapse, but are due to changes in the excitability of muscle innervation centers.
The found changes in central hemodynamics and vascular tone during anesthesia with ketamine indicate the excitation of cardiovasomotor formations of the reticular formation of the medulla oblongata, as a common source of the excitation system.
Comparison made effector manifestations of ketamine anesthesia with effector manifestations of the process central inhibition according to I.M. Sechenov clearly point to them. identity, which, in our opinion, is determined by the identity of neurophysiological mechanisms.
The beginning of the study of inhibition in the central unequal system is associated with the publication of the work of I.M. Sechenov "Reflexes of the brain", in which he showed the possibility of inhibition of the frog's motor reflexes during chemical stimulation of the visual tubercles of the brain.
Inhibition in the central nervous system - active nervous process, manifested in the suppression or weakening of the excitation process.
Central inhibition (experiment of I.M. Sechenov) - a process characterized by an increase in the time of the reflex or its complete absence, which occurs when a salt crystal is irritated by a cross section of the brain stem in the region of the visual halls.
Sechenov's classic experiment is as follows: in a frog with a cut brain at the level of the visual tubercles, the time of the flexion reflex was determined when the foot was irritated with sulfuric acid. After that, a salt crystal was placed on the optic tubercles and the reflex time was determined again. It gradually increased until the complete disappearance of the reaction. After removing the salt crystal and washing the brain with saline, the reflex time was gradually restored. This made it possible to say that inhibition is an active process that occurs when certain parts of the central nervous system are stimulated.
Later I.M. Sechenov and his students showed that inhibition in the CNS can occur when a strong stimulus is applied to any afferent pathways.
Peripheral inhibition was discovered by the Weber brothers in 1845. They found that irritation of the vagus nerve slows down the work of the heart until it stops completely.
Types and mechanisms of braking
Thanks to the microelectrode research technique, it became possible to study the process of inhibition at the cellular level.
There are two types of inhibition depending on the mechanisms of its occurrence: depolarization and hyperpolarization. Depolarizing inhibition occurs due to prolonged depolarization of the membrane, and hyperpolarizing - due to membrane hyperpolarization.
The onset of depolarization inhibition is preceded by a state of excitation. Due to prolonged stimulation, this excitation turns into inhibition. At the heart of the occurrence of depolarization inhibition is the inactivation of the membrane for sodium, as a result of which the action potential and its irritating effect on neighboring areas decrease, as a result, the conduction of excitation stops.
One of the types of this inhibition is pessimal, described by N.E. Vvedensky (1886), who showed that excitation can be replaced by inhibition in any area with low lability.
Hyperpolarization inhibition is carried out with the participation of special inhibitory structures and is associated with a change in the permeability of the membrane with respect to potassium and chlorine, which causes an increase in the membrane and threshold potentials, as a result of which the response becomes impossible.
Central inhibition (experiment of I.M. Sechenov): a — motor reflex to a painful stimulus; 6 - distribution of nerve impulses from inhibitory neurons of the brain stem to the spinal cord when a NaCl crystal is applied to the region of the visual halls and the absence of a motor reflex to a painful stimulus
Classification of types of CNS inhibition
Primary braking- the process of activation of inhibitory neurons that form synaptic connections with the cell to which inhibition is directed, while this process is primary for the cell, not associated with its preliminary excitation.
Secondary braking- a process that develops in a cell without the participation of specific inhibitory structures and is a consequence of its own excitation.
Outrageous braking - depletion of nerve cells under the action of high-intensity stimuli.
Pessimal inhibition- blocking of high-frequency impulses in unmyelinated nerve terminals due to their lower lability.
Presynaptic inhibition - a process that is realized when the axo-axonal inhibitory synapse is activated and blocks excitatory impulses directed to a given cell.
Post-synantic inhibition - a process that develops upon activation of axo-somatic and axo-dendritic inhibitory synapses and is localized on the cell's own membrane, to which inhibition is directed.
Reciprocal inhibition- mutual suppression of the activity of antagonistic nervous structures.
Afferent collateral inhibition - a special case of reciprocal inhibition, localized in the afferent part of the reflex arc.
Efferent collateral (return) inhibition- a process in which inhibitory interneurons act on the same nerve cells that activated them, while inhibition is the stronger, the more intense the previous excitation.
Lateral inhibition- a process in which intercalary inhibitory neurons suppress the activity of not only the cell that initiated them, but also other nearby ones.
Lateral inhibition (T - inhibitory neuron)
Recurrent inhibition (T-inhibitory intercalary neuron (Renshaw cell); M - motor neuron)
Reciprocal inhibition (T - inhibitory intercalary neuron (Renshaw cell); M - motor neuron)
Translational inhibition (T - inhibitory neuron)
Inhibition processes in the central nervous system
The processes of excitation and inhibition in the nervous system are closely interrelated.
Inhibition is a biological process aimed at weakening or preventing the occurrence of the excitation process. For the first time, the idea that in the CNS, in addition to excitation processes, there is an inhibition process, was put forward by I.M. Sechenov in 1862. In experiments on frogs with intact visual puffs, he analyzed the time of the flexion reflex. When salt crystals were placed on the visual hillock, the reflex time increased (inhibition). Subsequently, this type of inhibition was called "Sechenov's, or central, inhibition."
Inhibition in the central nervous system contributes to a certain coordination of the function performed. At the same time, the activity of neurons and centers that are not currently required to perform an adaptive reaction is blocked. In addition, inhibition also performs a protective function, protecting nerve cells from overexcitation and exhaustion under the action of strong stimuli.
There are several types of inhibition in the nervous system.
Postsypaptic inhibition develops when an inhibitory mediator released by a nerve ending changes the properties of the postsynaptic membrane in such a way that the nerve cell cannot generate an action potential. Postsypaptic inhibition may be due to prolonged depolarization or hyperpolarization that occurs in the postsynaptic membrane due to the interaction of the mediator with receptors that open potassium and chloride channels. The most common inhibitory mediators are gamma-aminobutyric acid and glycine. Glycine is secreted by special inhibitory cells (Renshaw cells) in the synapses formed by these cells on the membrane of another neuron. Acting on the postsynaptic membrane receptor, glycine increases its permeability for CI- ions, while chloride ions enter the cell according to the concentration gradient, resulting in hyperpolarization. Under the action of gamma-aminobutyric acid on the postsynaptic membrane, postsynaptic inhibition develops as a result of the entry of chloride ions into the cell or the exit of potassium ions from the cell. The concentration gradients of K + ions during the development of neuronal inhibition are maintained by the Na + /K + -pump, and those of CI - - CI - - by the pump.
Recurrent postsynaptic inhibition - this is such inhibition in which inhibitory interneurons (Renshaw cells) act on the same nerve cells that innervate them. An example of recurrent postsynaptic inhibition is inhibition in the motoneurons of the spinal cord. This type of inhibition provides, for example, alternate contraction and relaxation of the skeletal muscles - flexors and extensors, which is necessary for coordinating limb movements when walking.
Lateral postsynaptic inhibition due to the fact that inhibitory interneurons are connected in such a way that they are activated by impulses from an excited center and affect neighboring cells with the same functions. As a result, a very deep inhibition, called lateral inhibition, develops in these neighboring cells, since the resulting zone of inhibition is located on the side of the excited neuron and is initiated by it.
Reciprocal inhibition, an example of which is the inhibition of the nerve centers of the antagonist muscles, is that the excitation of the proprioreceptors of the flexor muscles simultaneously activates the motor neurons of these muscles and intercalary inhibitory neurons. Excitation of the intercalary neurons leads to postsynaptic inhibition of the motor neurons of the extensor muscles. If the centers of the flexor and extensor muscles were simultaneously excited, flexion of the limb in the joint would be impossible.
presynaptic inhibition due to the fact that a prolonged depolarization of the membrane can develop in the presynaptic ending, which leads to the development of inhibition. In the focus of depolarization, the process of propagation of excitation is disrupted and the impulses cannot pass through the zone of depolarization. Consequently, there is no release of the mediator into the synaptic cleft in sufficient quantities and the postsynaptic neuron is not excited. The CNS has a huge number of inhibitory neurons, in particular Renshaw cells. These inhibitory neurons synthesize specific inhibitory mediators and carry out the inhibitory response. Activation of an inhibitory neuron causes depolarization of the terminal membrane in afferent neurons, which makes it difficult for the action potential to be conducted. The mediator in such axonal synapses is gamma-aminobutyric acid or another inhibitory mediator. Depolarization is a consequence of an increase in the permeability of the membrane for chloride ions, as a result, these ions leave the cell.
