The manifestation and implementation of the 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, which is opposite in effect to the process of inhibition.
Almost until the middle of the 19th century, physiologists studied and knew only one nervous process - excitation.
The phenomena of inhibition in the 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 very formulation of the concept of reflex, since inhibition is necessarily involved in all nervous acts without exception. And .M.Sechenov discovered the phenomenon of central inhibition upon stimulation 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 nature these processes is one.
Inhibition is a local nervous process leading to inhibition or prevention of excitation. Inhibition is an active nervous process, the result of which is the limitation or delay of excitation. One of the characteristic features of the inhibitory process is the lack of the ability to actively spread through the nervous 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 and a type of electrical changes called inhibitory postsynaptic acid), which cause a special potential on the postsynaptic membrane (TPSP) or depolarization of the presynaptic nerve ending with which it contacts 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 a 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 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 neurotransmitter. 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 found out the mechanism of this phenomenon in the following experiment. He irritated the afferent nerve, causing excitation of the motor neuron that innervates the extensor muscle.
Nerve impulses, having reached the afferent neuron in the spinal ganglion, are sent along its axon in the spinal cord in two ways: to the motor neuron that innervates the extensor muscle, exciting it and along the collaters to the intermediate inhibitory neuron, the axon of which contacts the motor neuron that innervates the flexor muscle, thus causing inhibition of the antagonistic muscle. This type of inhibition was found in intermediate neurons of all levels of the central nervous system during the interaction of antagonistic centers. It has been called translational postsynaptic inhibition. This type of inhibition coordinates and distributes the processes of excitation and inhibition between the nerve centers.
Reverse (antidromic) postsynaptic inhibition (Greek antidromeo to run in the opposite direction) is the process of regulation by nerve cells of the intensity of the signals coming to them according to the principle of negative feedback. It lies in the fact that axon collaterals of a nerve cell establish synaptic contacts with special intercalary neurons (Renshaw cells), whose role is to act on neurons that converge on the cell that sends these axon collaterals. According to this principle, the inhibition of motor neurons is carried out.
The appearance of an impulse in a mammalian motor neuron not only activates muscle fibers, but also activates inhibitory Renshaw cells through axon collaterals. The latter establish synaptic connections with motor neurons. Therefore, an increase in motor neuron firing leads to greater activation of Renshaw cells, which causes 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 reflexively occurring in motor neurons.
The stronger the motor neuron is excited, 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. Therefore, there is a mechanism in the nervous system that protects neurons from excessive excitation. A characteristic feature of postsynaptic inhibition is that it is suppressed by strychnine and tetanus toxin (these pharmacological substances do not act on excitation processes).
As a result of the suppression of postsynaptic inhibition, the regulation of excitation in the central nervous system is disturbed, the excitation spreads ("diffuses") throughout the central nervous system, causing overexcitation of motor neurons and convulsive contractions of muscle groups (convulsions).
Reticular inhibition (lat. reticularis - mesh) is a nervous process that develops in spinal neurons under the influence of descending impulses from the reticular formation (giant reticular nucleus of the medulla oblongata). The effects created by reticular influences are functionally similar to the recurrent inhibition that develops on motor neurons. The influence of the reticular formation is caused by persistent IPSP, covering all motor neurons, regardless of their functional affiliation. In this case, as in the case of recurrent inhibition of motor neurons, their activity is limited. There is a certain interaction between this downward control from the reticular formation and the system of recurrent inhibition through Renshaw cells, and Renshaw cells are under constant inhibitory control from the two structures. The inhibitory influence from the reticular formation is an additional factor in the regulation of the level of motor neuron activity.
Primary inhibition can be caused by mechanisms of a different nature, not associated with changes in the properties of the postsynaptic membrane. Inhibition in this case 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 mediator secreted and released by presynaptic nerve endings with specific molecules of the postsynaptic membrane. The excitatory or inhibitory nature of the action of the mediator depends on the nature of the channels that open in the postsynaptic membrane. Direct proof of the presence of specific inhibitory synapses in the CNS was first obtained by D. Lloyd (1941).
Data on the electrophysiological manifestations of synaptic inhibition: the presence of a synaptic delay, the absence of an electric field in the region of synaptic endings gave reason to consider it a consequence of the chemical action of a special inhibitory mediator released by synaptic endings. D. Lloyd showed that if the cell is in a state of depolarization, then the inhibitory mediator causes hyperpolarization, while against the background of hyperpolarization of the postsynaptic membrane, it causes its depolarization.
presynaptic inhibition(Latin prae - ahead 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 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.
A characteristic feature of presynaptic depolarization is slow development and long duration (several hundred milliseconds), even after a single afferent impulse.
Presynaptic inhibition differs significantly from postsynaptic inhibition in pharmacological terms as well. Strychnine and tetanus toxin do not affect its course. However, narcotic substances (chloralose, nembutal) significantly enhance and lengthen 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 action is carried out at a point remote 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 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.
Secondary inhibition - inhibition carried out by the same nerve 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 the excitation of one group of nerve cells is carried out provide inhibition of other groups of cells through intercalary neurons. Reciprocal relations of excitation and inhibition in the CNS were discovered and demonstrated by N.E. Vvedensky: irritation of the skin on the hind leg in a frog causes its flexion and inhibition of flexion or extension on the opposite side. The interaction of excitation and inhibition is a common property of the entire nervous system and is found both in the brain and in the 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 CNS neurons.
General central inhibition is a nervous process that develops with any reflex activity and captures almost the entire central nervous system, including the centers of the brain. General central inhibition usually manifests itself before the occurrence of any motor reaction. It can manifest itself with such a small force of irritation at which there is no motor effect. This type of inhibition was first described by I.S. Beritov (1937). It provides a 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 an integral 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 there is a very massive simultaneous excitation of a large number of afferent pathways, as, for example, in traumatic shock.
Some researchers distinguish another type of inhibition - inhibition following excitation. It develops in neurons after the end of excitation as a result of a 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 a part of the nervous system that regulates the level of functional activity of internal organs, blood and lymphatic vessels, the secretory activity of the body's external and internal secretion glands.
The autonomic (autonomic) nervous system performs adaptive and trophic functions, actively participating in maintaining homeostasis(i.e. constancy of the environment) in the body. It adapts the functions of the internal organs and the entire human body to specific changes in the environment, affecting both the 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. Terminating in the skeletal muscles and in the skin, they regulate the level of metabolism in them, providing them with nutrition (trophism). The influence of the ANS also extends to the degree of sensitivity of the receptors. Thus, the autonomic nervous system covers more extensive areas of innervation than the somatic, since the somatic nervous system innervates only the skin and skeletal muscles, and the ANS regulates all internal organs and all tissues, performing adaptive-trophic functions in relation to everything body, including skin and muscles.
In its structure, the autonomic nervous system differs from the somatic. 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 with myelin sheath. The somatic nerve is formed, therefore, only by the processes of neurons, the bodies of which lie in the central nervous system. As for the nerves of the ANS, they are always formed two neurons. One - central, lies in the spinal cord or brain, the second (effector) - in the autonomic ganglion, and the nerve consists of two sections - preganglionic, usually covered with myelin sheath and therefore white, and postganglionic - not covered with myelin sheath and therefore gray colors. Their vegetative ganglia (always brought to the periphery from the CNS) 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 ( intramurally).
Some authors also highlight extramural ganglia that lie not in the wall, but close to the innervated organ. The farther the ganglia are located from the central nervous system, the greater part of the autonomic nerve is covered with a myelin sheath. And, therefore, the speed of transmission of the nerve impulse 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 mainly control the work of skeletal muscles, but we cannot control the contraction of smooth muscles (for example, the intestines). Unlike somatic, it does not have such a pronounced segmentality in innervation. The nerve fibers of the ANS exit the central nervous system from its three sections - the brain, thoracolumbar and sacral 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 CNS. As for the ANS, her 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 are of great importance, because. provide urgent adaptive reactions of innervated organs that do not require the participation of the central nervous system.
In 1863 I.M. Sechenov discovered the process of inhibition in the central nervous system.
Inhibition exists along with excitation and is one of the forms of neuron activity. braking called a special nervous process, expressed in a decrease or complete absence of a response to irritation.
The beginning of the study of inhibition in the central nervous system is associated with the publication of I.M. Secheny’s work “Reflexes of the Brain” (1863), in which he showed the possibility of inhibition of motor reflexes in a frog during chemical stimulation of the visual tubercles of the brain.
Sechenov's classic experience 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 central nervous system can occur when a strong stimulus is applied to any afferent pathways.
Types and mechanisms of inhibition. Thanks to the microelectrode research technique, it became possible to study the process of inhibition at the cellular level.
In the central nervous system, along with excitatory neurons, there are also inhibitory neurons. Each nerve cell has exciting And inhibitory synapses. And therefore, at any given moment on the body of a neuron, excitation occurs in some synapses, and inhibition in others; the ratio of these processes determines the nature of the response.
There are two types of inhibition depending on the mechanisms of its occurrence: depolarization 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. The basis for the occurrence of depolarization inhibition is the inactivation of the membrane by sodium, as a result of which the action potential and its irritating effect on neighboring areas decrease, and as a result, the conduction of excitation stops.
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.
According to the nature of occurrence, they are distinguished primary And secondary braking . Primary braking occurs under the influence of irritation immediately without prior excitation and is carried out with the participation of inhibitory synapses. Secondary braking is carried out without the participation of inhibitory structures and occurs as a result of the transition of excitation into inhibition.
Primary inhibition according to the mechanism of occurrence can be hyperpolarization and depolarization, and according to the place of occurrence - postsynaptic and presynaptic.
Primary hyperpolarizing postsynaptic inhibition characteristic of motor neurons and is carried out through an intercalary inhibitory neuron. The impulse that came to the inhibitory synapse causes hyperpolarization of the postsynaptic membrane of the motor neuron. At the same time, the MF value increases by 5-8 mV. This increase in MP is called inhibitory postsynaptic potential(TPSP). The magnitude and duration of the inhibitory postsynaptic potential depend on the strength of the stimulus and its interaction with the excitatory postsynaptic potential (EPSP).
Postsynaptic inhibition associated with the release of a neurotransmitter in the synapses, which changes the ion permeability of the postsynaptic membrane. The postsynaptic inhibition of a motor neuron, discovered by Ekklos and coworkers (1954), which occurs under the influence of Renshaw cells, has been well studied. Renshaw cells are located in the anterior horns of the spinal cord and are highly electrically active. They can even generate very high frequency potentials in response to a single presynaptic impulse - up to 1400 impulses per second. Excitation to Renshaw cells comes antidromic (in the opposite direction) along the branches of the axon of the motor neuron, which depart from it when it exits the spinal cord. In turn, the axon of the Renshaw cell contacts the soma of the same motor neuron. The excitation that came antidromic to the Renshaw cell causes a high-frequency discharge in it, under the influence of which an IPSP is created in the motor neuron, lasting up to 100 ms. This type of postsynaptic inhibition is called returnable or antidromic braking. Renshaw's cell mediator is acetylcholine.
Primary depolarization presynaptic inhibition
It develops in the presynaptic ramifications of axons of afferent neurons, to which the endings of intermediate neurons are suitable, forming axonal synapses on them. These neurons have high electrical activity. By sending high-frequency discharges, they create a long-term depolarization (up to several hundred milliseconds) on the presynaptic branches of afferent axons. In this regard, the conduction of impulses going to the synapses of motor neurons is blocked here, as a result of which their activity decreases or completely stops.
Presynaptic inhibition is a widespread mechanism in the CNS. It has been established that it can be caused not only by impulses with an afferent fiber, but also by stimulation of various brain structures.
Secondary braking is carried out without the participation of special inhibitory structures and develops in excitatory synapses. This type of inhibition was studied by N.E. Vvedensky (1886) and named pessimistic inhibition in any area with low lability (for example, in the neuromuscular synapse or in the synapses of the central nervous system). According to the mechanism of occurrence, secondary inhibition can be depolarization and hyperpolarization. Secondary depolarization inhibition is refractoriness and pessimal inhibition.
The mechanism of occurrence of pessimal inhibition has been studied in detail on neuromuscular synapses. It has been established that its development is based on persistent depolarization, which can occur both in the postsynaptic and in the presynaptic membrane of the synapse under the influence of frequent stimulation.
Secondary hyperpolarization inhibition occurs after excitation in the same neurons. With strong excitation of neurons, their AP is accompanied by subsequent long-term hyperpolarization, which occurs due to an increase in the permeability of the membrane for potassium. Therefore, the EPSP that occurs at a given strength of stimulation becomes insufficient to depolarize the membrane to a critical level. As a result, there is a decrease or lack of response.
The role of inhibition.
a. Protective role - to prevent the depletion of mediators and the cessation of the activity of the central nervous system.
b. Participates in the processing of information entering the central nervous system.
c. Inhibition is an important factor in ensuring the coordination activity of the central nervous system.
15. Coordinating activity of the central nervous system. mechanisms of coordination. Factors enabling coordination.
The concept of coordination. Adaptation of the body to various changes in the external environment is possible due to the presence of coordination of functions in the central nervous system. Under coordination understand the interaction of neurons, and, consequently, nervous processes, in the central nervous system, which ensures its coordinated activity aimed at integrating (combining) the functions of various organs and body systems.
There are a number of mechanisms underlying the coordinating activity of the nervous system. Some of them are related to the morphological features of its structure (the principle of a common final path, the principle of feedback), others are related to functional properties (irradiation, induction, etc.)
Irradiation of excitation in the central nervous system. In 1908, A. A. Ukhtomsky and N. E. Vvedensky, in their joint work, established that any excitation that occurs when a particular receptor is irritated, having come to the central nervous system, spreads widely through it - radiates. It captures not only the centers of this reflex, but also other parts of the central nervous system. The irradiation is the wider, the stronger and longer afferent irritation.
Irradiation is based on numerous connections of axons of afferent neurons with dendrites and bodies of CNS neurons, which have a large number of contacts with various nerve centers and with each other. Excitation can spread over long distances: from the neurons of the spinal cord to various parts of the brain up to the cerebral cortex.
Experimental data have been obtained that make it possible to speak about the regularities of irradiation. It turned out that, first of all, neurons with the smallest threshold potential are involved in the reaction, i.e. with the highest excitability. In them, first of all, depolarization reaches a critical level and a wave of excitation occurs. With an increase in the intensity of stimulation, less excitable neurons are involved in the reaction, while the excitation process captures an increasing number of CNS cells.
But, despite the wide connection of nerve centers, the irradiation of excitation in the central nervous system has its limits, as a result of which only certain of its departments come into an active state.
Induction processes in the CNS. Induction- one of the most important principles of coordination, which consists in the fact that when excitation occurs in one of the sections of the central nervous system, the opposite process occurs in the conjugated centers - inhibition. And, conversely, when inhibition occurs in some centers, excitation occurs in conjugated ones. Induction limits the process of irradiation.
Distinguish between simultaneous (or spatial) and sequential induction. At simultaneous induction at the same time, a process of excitation occurs in one center, and inhibition occurs in the conjugated center (or vice versa). An example of simultaneous induction can be the reciprocal innervation of antagonist muscles discussed above.
The processes occurring in the central nervous system are characterized by great mobility, without which it is impossible to carry out complex and fast motor acts and other responses. In the same center, the processes occurring in it are changed to the opposite ones. The change of arousal is called negative series induction, and inhibition on excitation - positive sequential induction. Due to such a successive change of processes in the nerve centers, alternation of flexion and extension reactions of the limbs is possible, which is necessary for the implementation of a motor act.
Convergence. Impulses coming to the CNS through various afferent fibers can converge (converge) to the same intermediate and effector neurons. This fact formed the basis of the principle of convergence established by C. Sherrington. The convergence of nerve impulses is explained by the fact that the axons of many other nerve cells terminate on the body and dendrites of each neuron in the CNS. In the spinal cord and medulla oblongata, convergence is relatively limited: on intercalary and motor neurons, afferent impulses converge, arising in different parts of the receptive field of only one and the same reflex. In contrast, in the higher parts of the CNS - in the subcortical nuclei and in the cerebral cortex - there is a convergence of impulses emanating from different receptor zones. Therefore, the same neuron can be excited by impulses arising from stimulation of auditory, visual, and skin receptors.
The principle of a common final path. This principle comes from the anatomical relationship between afferent and efferent neurons. The number of sensory neurons that bring excitation to the central nervous system is 5 times greater than the number of motor neurons. The ratio between them will be even greater if we take into account that the interneurons are receptive neurons in the CNS. In this regard, many impulses from various receptors come to one motor neuron, but only some of them acquire a working value. Thus, a wide variety of stimuli can cause the same reflex reaction, i.e. there is a struggle for a “common final path”. Later it was shown that it is not the quantitative ratio of the paths, but the functional characteristics of the nerve centers that determine which of the many nerve impulses colliding on the way to the motor neuron will be the winner and take possession of the common final path. In response to many different stimuli, a reaction that is biologically more significant for the body always occurs.
Feedback principle. The influence of a working body on the state of its center is called feedback. It provides long-term maintenance of the activity of nerve centers, the movement of excitation and inhibition processes in the central nervous system and depends on a constant influx of secondary afferent impulses. Impulses that arise as a result of the activity of various organs and tissues are called, secondary afferent impulses, and the impulses coming from the receptors and causing the primary reflex act - primary reflex impulses.
Secondary afferent impulses arise in muscles, tendons and joints during their activity. They, constantly coming from all organs of the body to the central nervous system, contribute to the sensation of the position of our body without visual control, ensure the maintenance of the desired level of functioning of neurons at any given moment.
Secondary afferent impulsation makes constant corrections to the ongoing reflex act and ensures the most subtle adaptation of the organism to external influences.
Afferent impulses coming from the working organs contribute to the creation autogenic (own) inhibition. It arises as a result of the receipt of afferent impulses from the receptors - Golgi tendon receptors - into the central nervous system. These receptors are activated when the muscles are stretched or contracted. The resulting IPSP reduces the degree of activity of this motor neuron. The magnitude of these changes may vary. Autogenic inhibition provides the best adaptation of the muscle to the implementation of the reflex motor act.
Factors enabling coordination:
1) Factor of structural-functional connection - this is the presence between the departments of the central nervous system, between the central nervous system and various organs of a functional connection, which ensures the predominant distribution of excitation between them. direct connection- control of another center or working organ by sending efferent impulses to them, PR: the cerebellum sends impulses to the nuclei of the brain stem. Feedback (reverse afferentation) - control of the nerve center or working organ with the help of afferent impulses coming from them. Reciprocal connection- provides inhibition of the antagonist center when the agonist center is excited (flexor and extensor muscles).
2) Subordination factor - subordination of the underlying departments of the central nervous system to the overlying ones.
3) Force factor. The principle of a common final path - in the struggle for a common final path, a stronger excitation wins (a more biologically important team), PR: with weak irritation - a scratching reflex, with strong - a defensive reflex flexion of the limb, with simultaneous irritation, only a defensive reflex arises).
4) Unilateral conduction of excitation in chemical synapses regulates the spread of excitement.
5) The Phenomenon of Relief participates in the development of skills - excitement spreads faster along the beaten paths, skills become more coordinated, unnecessary movements are gradually eliminated.
6) Dominant plays an important role in coordination processes. Provides automated performance of motor acts in the course of labor activity (dominant of motor centers).
The continuous change in the processes of excitation and inhibition in the cortical cells determines the cyclicity of the work of individual organs and the whole organism as a whole. This explains the sometimes seemingly incredible performance of some outstanding people; No wonder they say that 90% of genius lies in high working capacity, which largely depends on a rational system of work. Such a deeply thought-out system, as a rule, was created for themselves by all outstanding people.
Braking- an active process that occurs under the action of stimuli on the tissue, manifests itself in the suppression of another excitation, there is no functional administration of the tissue.
Inhibition can only develop in the form of a local response.
There are two braking type:
1) primary. For its occurrence, the presence of special inhibitory neurons is necessary. Inhibition occurs primarily without prior excitation under the influence of an inhibitory mediator. There are two types of primary inhibition:
presynaptic in the axo-axonal synapse;
postsynaptic at the axodendrial synapse.
2) 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:
beyond, arising from a large flow of information entering the cell. The flow of information lies outside the neuron's performance;
pessimal, arising at a high frequency of irritation; parabiotic, arising from strong and long-acting irritation;
inhibition following excitation, resulting from a decrease in the functional state of neurons after excitation;
braking by the principle of negative induction;
inhibition of conditioned reflexes.
The processes of excitation and inhibition are closely related, occur simultaneously and are different manifestations of a single process. The foci of excitation and inhibition are mobile, cover larger or smaller areas of neuronal populations, and may be more or less pronounced. Excitation will certainly be replaced by inhibition, and vice versa, i.e., there are inductive relations between inhibition and excitation.
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.
In 1862, I. M. Sechenov discovered the phenomenon central braking. He proved in his experiment that irritation of the frog's optic tubercles with a sodium chloride crystal (the large hemispheres of the brain were removed) causes inhibition of spinal cord reflexes. After elimination of the stimulus, the reflex activity of the spinal cord was restored. The result of this experiment allowed I. M. Secheny to conclude that in the CNS, 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 principle of negative induction underlies the phenomenon of inhibition: a more excitable section in the central nervous system inhibits the activity of less excitable sections.
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-motor neurons 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 can be glycine, GABA and a number of other substances. Usually, glycine is produced in synapses, with the help of which postsynaptic inhibition is carried out. When glycine as a mediator interacts with neuron glycine receptors, hyperpolarization of the neuron occurs ( TPSP) and, as a result, a decrease in the excitability of the neuron up to its complete refractoriness. As a result, excitatory influences provided through other axons become ineffective or ineffective. The neuron is switched off from work completely.
Inhibitory synapses open mainly chloride channels, which allows chloride ions to easily pass through the membrane. To understand how inhibitory synapses inhibit the postsynaptic neuron, we need to remember what we know about the Nernst potential for Cl- ions. We calculated that it is equal to approximately -70 mV. This potential is more negative than the resting membrane potential of the neuron, which is -65 mV. Therefore, the opening of chloride channels will facilitate 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 about -70 mV.
The opening of potassium channels allows positively charged K+ ions to move outward, resulting in more negativity within 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 exit of negativity values beyond the initial resting membrane potential is called TPSP.
VNS provides extraorganic and intraorganic regulation of body functions and includes three components: 1) sympathetic; 2) parasympathetic; 3) metsympathetic.
The autonomic nervous system has a number of anatomical and physiological features that determine the mechanisms of its work.
Anatomical properties:
1. Three-component focal arrangement of nerve centers. The lowest level of the sympathetic section is represented by the lateral horns from the VII cervical to 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 nuclei of the hypothalamus (the sympathetic division is the posterior group, and the parasympathetic division is the anterior one). The cortical level lies in the region of the sixth-eighth Brodmann fields (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 internal organs does not reach the threshold of our consciousness.
2. The presence of autonomic ganglia. In the sympathetic department, they are located either on both sides along the spine, or are part of the plexus. Thus, the arch has a short preganglionic and a long postganglionic path. The neurons of the parasympathetic department 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 group B and C.
Physiological properties:
1. Features of the functioning of the autonomic ganglia. The presence of the phenomenon cartoons(simultaneous occurrence of two opposite processes - divergence and convergence). Divergence- the 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 transmission of information from the central nervous system to the working body. 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. Thus, they regulate the flow of information from the CNS. Due to this property, they are called nerve centers placed 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 division is represented by preganglionic fibers, and the parasympathetic pathway 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 carries out the innervation of all organs and tissues (stimulates the work of 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 consists in maintaining the constancy of the internal environment of the body in an active state, i.e. the sympathetic nervous system is included in the work only during physical exertion, emotional reactions, stress, pain effects, blood loss.
Adaptive-trophic function aimed at regulating the intensity of metabolic processes. This ensures the adaptation of the organism to the changing conditions of the environment of existence.
Thus, the sympathetic department begins to act in an active state and ensures the functioning of organs and tissues.
parasympathetic nervous system is a sympathetic antagonist and performs homeostatic and protective functions, regulates the emptying of hollow organs.
The homeostatic role is restorative and operates at rest. This manifests itself in the form of a decrease in the frequency and strength of heart contractions, stimulation of the activity 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 causes food to be expelled, etc.
Emptying of hollow organs occurs with an increase in the tone of smooth muscles that make up the wall. This leads to the entry of nerve impulses into the central nervous system, where they are processed and sent along the effector path to the sphincters, causing them to relax.
Metsympathetic nervous system is a collection of microganglia located in the tissues of organs. They consist of three types of nerve cells - afferent, efferent and intercalary, therefore, they perform the following functions:
20. Functional features of the somatic and autonomic nervous system. Comparative characteristics of the sympathetic, parasympathetic and metasympathetic divisions of the autonomic nervous system.
The first and main difference between the ANS structure and the somatic structure is the location of the efferent (motor) neuron. In the SNS, the intercalary and motor neurons are located in the gray matter of the SC; in the ANS, the effector neuron is located on the periphery, outside 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 completely located in the intramural ganglia and nerve plexuses of the internal organs.
The second difference concerns the exit of nerve fibers from the CNS. Somatic NIs leave the SC segmentally and cover at least three adjacent segments with innervation. The fibers of the ANS exit from three parts of the CNS (GM, thoracolumbar and sacral SM). They innervate all organs and tissues without exception. Most visceral systems have triple (sympathetic, para- and metasympathetic) innervation.
The third difference concerns the innervation of the somatic and ANS organs. Transection of the ventral roots of the SM in animals is accompanied by a complete regeneration of all somatic efferent fibers. It does not affect the arcs 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 this neuron. It is this circumstance that emphasizes the relative autonomy of this section of the National Assembly.
The fourth difference relates to the properties of nerve fibers. In the ANS, they are mostly non-fleshy or thin fleshy, such as preganglionic fibers, the diameter of which does not exceed 5 microns. 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, fleshy, 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 needed than for motor somatic fibers. ANS fibers are characterized by a long refractory period and a large chronaxy. The speed of NI propagation along them is low and amounts to up to 18 m/s in preganglionic fibers, and up to 3 m/s in postganglionic fibers. The action potentials of the ANS fibers are characterized by a longer duration than in somatic efferents. Their occurrence in preganglionic fibers is accompanied by a prolonged trace positive potential, in postganglionic fibers - by a trace negative potential followed by prolonged trace hyperpolarization (300-400 ms).
provides intraorganic innervation;
are an intermediate link between the tissue and the extraorganic nervous system. Under the action of a weak stimulus, the metsympathetic department is activated, and everything is decided at the local level. When strong impulses are received, they are transmitted through the parasympathetic and sympathetic divisions to the central ganglia, where they are processed.
The metsympathetic nervous system regulates the work of smooth muscles that are part of most organs of the gastrointestinal tract, myocardium, secretory activity, local immunological reactions, etc.
Inhibition in the central nervous system is a special nervous process caused by excitation and manifested in the suppression of another excitation.
Primary postsynaptic inhibition- inhibition, unrelated to the initial process of excitation and developing as a result of the activation of special inhibitory structures. Inhibitory synapses form an inhibitory mediator at their endings (GABA, glycine; in some CNS synapses, acetylcholine can play the role of an inhibitory mediator). An inhibitory postsynaptic potential (IPSP) develops on the postsynaptic membrane, which reduces the excitability of the membrane of the postsynaptic neuron. Only interneurons can serve as inhibitory neurons; afferent neurons are always excitatory. Depending on the type of inhibitory neurons and the structural organization of the neural network, postsynaptic inhibition is divided into:
- 1. Reciprocal inhibition. It underlies the functioning of antagonist muscles and ensures muscle relaxation at the moment of contraction of the antagonist muscle. An afferent fiber that conducts excitation from muscle proprioceptors (for example, flexors) in the spinal cord is divided into two branches: one of them forms a synapse on the motor neuron that innervates the flexor muscle, and the other on the intercalary, inhibitory, forming an inhibitory synapse on the motor neuron that innervates extensor muscle. As a result, excitation coming along the afferent fiber causes excitation of the motor neuron innervating the flexor and inhibition of the motor neuron of the extensor muscle.
- 2. Reverse braking. It is realized through inhibitory Renshaw cells, open in the spinal cord. The axons of the motor neurons of the anterior horns give off a collateral to the Renshaw inhibitory neuron, whose axons return to the same motor neuron, forming inhibitory synapses on it. Thus, a circuit with negative feedback is formed, which makes it possible to stabilize the frequency of motoneuron discharges.
- 3. Central (Sechenov) inhibition. It is carried out by inhibitory intercalary neurons, through which the effect on the motor neuron of the spinal cord is realized, the excitation that occurs in the visual tubercles under the influence of their irritation. On the motor neuron of the spinal cord, EPSPs that occur in the pain receptors of the limb and TPSP that occur in inhibitory neurons under the influence of excitation of the thalamus and the reticular formation are summarized. As a result, the time of the protective flexion reflex increases.
- 4. Lateral inhibition is carried out using inhibitory intercalary neurons in parallel neural networks.
- 5. Primary presynaptic inhibition develops in the terminal sections of axons (before the presynaptic structure) under the influence of special axo-axonal inhibitory synapses. The mediator of these synapses causes depolarization of the membrane of the terminals and brings them into a state similar to Verigo's cathodic depression. The membrane in the area of such a lateral synapse prevents the conduction of action potentials to the presynaptic membrane, the activity of the synapse decreases.
Presynaptic inhibition is a decrease or shutdown of cell activity due to synaptic inhibition of the excitatory terminal ending on it. The phenomenon of presynaptic inhibition was fixed by Gasser and Graham in 1933, observing the effect of the development of inhibition of flexion reflexes upon stimulation of other roots. This type of inhibition was first termed presynaptic inhibition by Frank and Fuortes in 1957.
An increase in the frequency of preliminary stimuli changes the nature of the suppression. In particular, one series of stimulation at a frequency of 200-300 pulses per second causes a maximum suppression of less than 10%, and two series - a suppression of less than 20%. During presynaptic inhibition, the suppression of monosynaptic EPSP is not associated with any changes in their temporal parameters.
Inhibitory synapses at the ends of the fibers provide a fairly significant depolarization, called the depolarization of the primary afferents, or primary efferent depolarization (PAD). In the spinal cord, PAD exhibits a long phase (up to 25 ms) of rise to a rounded apex and is characterized by a longer duration compared to postsynaptic processes. The long duration of PAD is explained either by the prolonged action of the mediator, or by a slow, passive decrease in depolarization due to the large electrical time constant of the membrane. The passively decreasing PAD component is removed by an impulse propagating along the afferent fiber to its central endings.
There is a correspondence in all respects between the observed depolarization of the primary afferent fibers and the suppression of their synaptic excitatory action.
Presynaptic depolarization of afferents reduces the magnitude of their presynaptic spike potential and thus reduces the EPSP it causes. According to Katz (1962), a decrease in the spike potential by 5 mV leads to a decrease in the release of mediator quanta and to a decrease in EPSP to 50% or less.
The nature of PAD in different neurons differs in its characteristics. In general, the time parameters are comparable. PAD of cutaneous nerve fibers is characterized by a larger amplitude for single stimuli with a shorter latent period (about 2 ms), the maximum is also reached earlier than in the case of PAD caused by rhythmic stimulation of nerve fibers coming from the muscles. PAP in the sphenoid nucleus has a short latent period (about 2 ms) and a rapid rise to a maximum.
Inhibitory synapses are chemical in nature; GABA serves as a mediator in them. Depolarization of the primary afferents inactivates excitatory sodium channels. Shunting of sodium channels reduces the amplitude of the presynaptic action potential. As a result, synaptic transmission of the motor impulse is weakened or eliminated.
In all types of excitatory synapses, a close relationship is found between depolarization of presynaptic fibers and inhibition of synaptic transmission. This inhibition affects not only local spinal reflexes, but also synaptic transmission in ascending pathways from both cutaneous and spinocerebellar afferents. In addition, presynaptic inhibition affects the synaptic transmission of the posterior columns to the nuclei of the tender and sphenoid bundles. Descending impulses from the cerebral cortex and brainstem also have a presynaptic inhibitory effect on group fibers and cutaneous afferent fibers in the spinal cord and sphenoid nucleus. Presynaptic inhibition of secondary afferent fibers extending from the sphenoid nucleus and having a switch in the thalamus was found. Synapses with presynaptic inhibition were found in the thalamus-associated nucleus of the brain - the lateral geniculate body. No synaptic structures were found in the cerebral cortex that could carry out presynaptic inhibition. At these higher levels of the nervous system, postsynaptic inhibition dominates. Presynaptic inhibition acts as a negative feedback, reducing the flow of sensory information into the central nervous system. Typically, this negative feedback does not have a precise topography, but is usually concentrated within a single sensory modality. Presynaptic inhibition serves as a mechanism for regulating the motor systems of the spinal cord. Its feature is the possibility of a specific effect on individual synaptic inputs without changing the excitability of the entire cell. Thus, redundant information is eliminated even before it reaches the site of integration of the cell body of the neuron.
Secondary braking is not associated with inhibitory structures, is a consequence of previous excitation. Pessimal inhibition (discovered by N.E. Vvedensky in 1886) develops in polysynaptic reflex arcs with excessive activation of central neurons and plays a protective role. It is expressed in persistent depolarization of the membrane, leading to inactivation of sodium channels. Inhibition following excitation develops in neurons immediately after the action potential and is typical for cells with long-term trace hyperpolarization. Thus, the processes of inhibition in local neural networks reduce excessive activity and are involved in maintaining optimal modes of neuron activity.
Mechanisms for coordinating reflex activity: reciprocal innervation, dominant (A.A. Ukhtomsky), principles of feedback and a common final path, the principle of subordination.
The principle of irradiation of excitation. Irradiation - distribution, expansion of the reflex response. This is the phenomenon of “spreading” of excitation through the neurons of the central nervous system, which develops either after the action of a superstrong stimulus, or against the background of inhibition being turned off. The spread of excitation is possible due to numerous contacts between neurons that occur during the branching of axons and dendrites of intercalary neurons. Irradiation allows you to increase the number of muscle groups involved in the reflex response. Irradiation is limited by inhibitory neurons and synapses.
Against the background of the action of strychnine, which blocks inhibitory synapses, generalized convulsions occur with tactile stimulation of any part of the body or with irritation of the receptors of any sensory system. In the cerebral cortex, the phenomenon of irradiation of the inhibition process is observed.
The coordination of reflex acts is based on certain mechanisms based on the structural and functional organization of the central nervous system and referred to as the “principles” of the formation of a reflex response.
The principle of reciprocal innervation. Reciprocal (conjugate) coordination was discovered by N.E. Vvedensky in 1896. Due to reciprocal inhibition, i.e. activation of one reflex is simultaneously accompanied by inhibition of the second, opposite in its physiological essence.
The principle of a common "final path". Opened by the English physiologist C. Sherrington (1906). One and the same reflex (for example, muscle contraction) can be caused by irritation of various receptors, since the same terminal - the motor neuron of the anterior horns of the spinal cord is part of many reflex arcs. Reflexes, the arcs of which have a common final path, are divided into agonistic and antagonistic. The former reinforce, the latter inhibit each other, as if competing for the final result. Reinforcement is based on convergence and summation, competition for the final path is based on coupled inhibition.
Feedback principle. Any reflex act is controlled by feedback from the center. Feedback consists in secondary afferentation entering the central nervous system from receptors that are excited when the functional activity of the working organ changes. For example, action potentials due to excitation of receptors in muscles, tendons, and articular capsules of a flexing limb, during the act of flexion, enter all structures of the central nervous system, starting from the centers of the spinal cord. A distinction is made between positive feedback (which reinforces the reflex, which is the source of reverse afferentation) and negative feedback, when the reflex that causes it is inhibited. Feedback underlies the self-regulation of body functions.
The principle of return. The phenomenon of recoil consists in the rapid change of one reflex by another of the opposite value. For example, after flexion of a limb, its extension is faster, especially if the flexion was strong. The mechanism of this phenomenon is that with a strong contraction of the muscles, the Golgi receptors of the tendons are excited, which, through inhibitory interneurons, inhibit the motoneurons of the flexor muscles and form a branch that excites the center of the extensor muscles. Thanks to this mechanism, you can get the sum of reflexes - chain reflexes (the end of one reflex response initiates the next) and rhythmic (multiple repetition of rhythmic movements).
dominance principle. The final behavioral effect in the coordination of reflexes can be changed depending on the functional state of the centers (the presence of dominant foci of excitation).
Features of the dominant focus of excitation:
- 1. Increased excitability of neurons.
- 2. Persistence of the excitation process.
- 3. The ability to summation of excitation.
- 4. Inertia. The focus dominates, suppresses neighboring centers by conjugated inhibition, being excited at their expense. The dominant can be obtained by chemical action on the centers, for example, with strychnine. Dominant excitation is based on the ability of the excitatory process to irradiate along neural circuits.
Physiology is a science that gives us an idea of the human body and the processes taking place in it. One of these processes is the inhibition of the CNS. It is a process that is generated by excitation and is expressed in the prevention of the appearance of another excitation. This contributes to the normal functioning of all organs and protects the nervous system from overexcitation. Today, there are many types of inhibition that play an important role in the functioning of the body. Among them, reciprocal inhibition (combined) is also distinguished, which is formed in certain inhibitory cells.
Types of central primary braking
Primary inhibition is observed in certain cells. They are found near inhibitory neurons that produce neurotransmitters. In the CNS, there are such types of primary inhibition: recurrent, reciprocal, lateral inhibition. Let's see how each of them works:
- Lateral inhibition is characterized by the inhibition of neurons by the inhibitory cell that is located near them. Often this process is observed between such neurons of the retina as bipolar and ganglionic. This helps to create conditions for a clear vision.
- Reciprocal - characterized by a mutual reaction, when some nerve cells produce inhibition of others through the intercalary neuron.
- Reverse - is caused by inhibition of the neuron of the cell, which inhibits the same neuron.
- Return relief is characterized by a decrease in the reaction of other inhibitory cells, in which the destruction of this process is observed.
In simple CNS neurons, inhibition occurs after excitation, traces of hyperpolarization appear. Thus, reciprocal and recurrent inhibition occurs due to the inclusion in the circuit of the spinal reflex of a special inhibitory neuron, which is called the Renshaw cell.
Description
Two processes are constantly working in the central nervous system - inhibition and excitation. Inhibition is aimed at stopping or weakening certain activities in the body. It is formed when two excitations meet - inhibitory and inhibitory. R interciprocal inhibition is one in which the excitation of some nerve cells inhibits other cells through an intermediate neuron, which has a connection only with other neurons.
Experimental discovery
Reciprocal inhibition and excitation in the CNS were identified and studied by N.E. Vedensky. He did an experiment on a frog. Excitation was carried out on the skin of her hind limb, which caused bending and straightening of the limb. Thus, the coherence of these two mechanisms is a common feature of the entire nervous system and is observed in the brain and spinal cord. It was found in the course of experiments that the performance of each action of movement is based on the relationship of inhibition and excitation on the same nerve cells of the central nervous system. Vvedensky N.V. said that when excitation occurs at any point of the central nervous system, induction appears around this focus.
Combined inhibition according to Ch. Sherrington
Sherrington C. claims to ensure complete coordination of limbs and muscles. This process allows the limbs to bend and straighten. When a person reduces a limb, excitation is formed in the knee, which passes into the spinal cord to the center of the flexor muscles. At the same time, a deceleration reaction appears in the center of the extensor muscles. This happens and vice versa. This phenomenon is triggered during motor acts of great complexity (jump, run, walk). When a person walks, he alternately bends and straightens his legs. When the right leg is bent, excitation appears in the center of the joint, and the process of inhibition occurs in a different direction. The more complex the motor acts, the greater the number of neurons that are responsible for certain muscle groups are in reciprocal relationships. Thus, it arises due to the work of the intercalary neurons of the spinal cord, which are responsible for the process of inhibition. The coordinated relationships of neurons are not constant. The variability of the relationship between the motor centers makes it possible for a person to make difficult movements, for example, to play musical instruments, dance, and so on.
Reciprocal inhibition: scheme
If we consider this mechanism schematically, then it has the following form: the stimulus that comes from the afferent part through the usual (intercalary) neuron causes excitation in the nerve cell. The nerve cell sets the flexor muscles in motion, and through the Renshaw cell, it inhibits the neuron, which causes the extensor muscles to move. This is how the coordinated movement of the limb proceeds.
Extension of the limb occurs in reverse. Thus, it ensures the formation of reciprocal relationships between the centers of the nerves of certain muscles thanks to Renshaw cells. Such inhibition is physiologically practical as it makes it easy to move the knee without any auxiliary control (voluntary or involuntary). If this mechanism did not exist, then there would be a mechanical struggle of human muscles, convulsions, and not coordinated acts of movement.
The essence of combined inhibition
Reciprocal inhibition allows the body to make arbitrary movements with the limbs: both easy and quite complex. The essence of this mechanism lies in the fact that the nerve centers of the opposite action are simultaneously in the opposite state. For example, when the inspiratory center is stimulated, the expiratory center is inhibited. If the vasoconstrictor center is in an excited state, then the vasodilating center is in a inhibited state at this time. Thus, the conjugated inhibition of the centers of reflexes of the opposite action ensures the coordination of movements and is carried out with the help of special inhibitory nerve cells. A coordinated flexion reflex occurs.
Wolpe braking
Wolpe in 1950 formulated the assumption that anxiety is a stereotype of behavior, which is fixed as a result of reactions to situations that cause it. The connection between stimulus and response can be weakened by a factor that inhibits anxiety, such as muscle relaxation. Wolpe called this process "". It underlies today the method of behavioral psychotherapy - systematic desensitization. During it, the patient is introduced into many imagined situations, while muscle relaxation is caused with the help of tranquilizers or hypnosis, which reduces the level of anxiety. As the absence of anxiety becomes fixed in mild situations, the patient moves on to difficult situations. As a result of therapy, a person acquires the skills to independently control disturbing situations in reality using the muscle relaxation technique that he has mastered.
Thus, reciprocal inhibition was discovered Wolpe and is widely used today in psychotherapy. The essence of the method lies in the fact that there is a decrease in the strength of a certain reaction under the influence of another, which was caused simultaneously. This principle is at the heart of cont-conditioning. Combined inhibition is due to the fact that the reaction of fear or anxiety is inhibited by an emotional reaction that occurs simultaneously and is incompatible with fear. If such inhibition occurs periodically, then the conditional connection between the situation and the anxiety reaction weakens.
Wolpe method of psychotherapy
Joseph Wolpe pointed out that habits tend to fade when new habits develop in the same situation. He used the term "reciprocal inhibition" to describe situations where the appearance of new reactions leads to the extinction of previously occurring reactions. So, with the simultaneous presence of stimuli for the appearance of incompatible reactions, the development of a dominant reaction in a certain situation presupposes a conjugated inhibition of others. Based on this, he developed a method for treating anxiety and fears in people. This method involves finding those reactions that are suitable for the occurrence of reciprocal inhibition of fear reactions.
Wolpe singled out the following reactions that are incompatible with anxiety, the use of which will make it possible to change a person's behavior: assertive, sexual, relaxation and "anxiety relief" reactions, as well as respiratory, motor, drug-enhanced reactions and those caused by conversation. Based on all this, various techniques and techniques have been developed in psychotherapy in the treatment of anxious patients.
Results
Thus, to date, scientists have explained the reflex mechanism that uses reciprocal inhibition. According to this mechanism, nerve cells excite inhibitory neurons that are located in the spinal cord. All this contributes to the coordinated movement of the limbs in humans. A person has the ability to perform various complex motor acts.
