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Inhibitory postsynaptic potential is. Inhibitory postsynaptic potential. The principle of reflex work

An excitatory postsynaptic potential (EPSP) occurs in the case of a strong incoming flow of Na + ions and a weaker outgoing current of K + ions as a result of the opening of nonspecific channels during the interaction of the mediator with the corresponding receptor on the postsynaptic membrane.

The ion currents involved in the occurrence of EPSPs behave differently than the Na + and K + currents during action potential generation. This is due to the fact that other ion channels with different properties are involved in the mechanism of EPSP formation. When an action potential is formed, voltage-gated ion channels are activated, which open further channels with increasing depolarization, so that the depolarization process reinforces itself. The conductance of ion channels on the postsynaptic membrane depends only on the number of mediator molecules bound to the receptor molecules and, consequently, on the number of open ion channels (transmitter-gated or ligand-gated channels). The amplitude of the EPSP lies in the range from 100 μV to 10 mV. Depending on the type of synapse, the total duration of EPSP is in the range from 5 to 100 ms. In the synapse zone, the locally formed EPSP passively (electrotonically) propagates throughout the entire postsynaptic membrane of the cell. This distribution is not subject to the all-or-nothing law. If a large number of synapses are excited simultaneously or almost simultaneously, then a phenomenon occurs summation, which manifests itself in the form of the appearance of an EPSP of a significantly larger amplitude, which can depolarize the membrane of the entire postsynaptic cell. If the magnitude of this depolarization reaches a certain threshold in the area of ​​the postsynaptic membrane (10 mV and higher), then voltage-controlled Na + channels open very quickly on the axon hillock of the nerve cell and it generates an action potential that propagates along its axon. In the case of the motor end plate, this results in muscle contraction. From the beginning of the EPSP to the formation of the action potential, another 0.3 ms passes. With abundant release of the transmitter (mediator), the postsynaptic potential may appear as early as 0.5-0.6 ms after the action potential that has arrived in the presynaptic region. Synaptic delay time (the time between the occurrence of pre- and postsynaptic action potential) always depends on the type of synapse.

Some other substances that affect transmission in the synapse.
Other compounds may also have a high affinity for the receptor protein. If their binding to the receptor leads to the same effect as the mediator, they are called agonists if these compounds by binding, on the contrary, prevent the action of mediators - antagonists. For most synapses, a number of endogenous and exogenous compounds have been established that are capable of interacting with the binding site of the postsynaptic membrane. Many of them are drugs. For example, for a cholinergic synapse (transmitter - Ach) agonist is an succinylcholine, it, like Ach, contributes to the emergence of EPSP. Along with the d-tubocurarine(contained in the poison curare) refers to antagonists. It is a competitive blocker for nicotinic receptors.

2.6. Ion channel opening mechanism in metabotropic
receptors

In contrast to synapses (for example, nicotinic synapses), in which the transmitter opens an ion channel, there are other receptor proteins that are not ion channels. An example is the muscarinic-type cholinergic synapse. The name of the synapse was acquired by the action of the agonist - the poison of the fly agaric muscarine. In this synapse, the Ach-receptor
the torus is a protein. This protein has a great chemical similarity with the light-sensitive pigment rhodopsin, α- and β-adrenergic and other receptors. The ion channels necessary for the emergence of EPSPs open there only due to metabolic processes. Therefore, their function includes metabolic processes, and these receptors are called metabotropic. The process of excitation transfer in this synapse occurs as follows (Fig. 1.5, 1.8). Once the mediator binds to the receptor, the G protein, which has three subunits, forms a complex with the receptor. In this, rhodopsin, the muscarinic receptor, and all other G protein-coupled receptors are similar to each other. GDP bound to the G-protein is replaced by GTP. In this case, an activated G-protein is formed, consisting of GTP and an α-subunit, which opens the potassium ion channel.

There are many opportunities for second messengers to influence ion channels. With the help of second messengers, certain ion channels can open or close. Along with the channel opening mechanism described above, GTP can also activate β- and γ-subunits in many synapses, for example, in the heart. Other synapses may involve other second messengers. Thus, ion channels can be opened by cAMP / IP 3 or protein kinase C phosphorylation. This process is again associated with G-protein
lump, which activates phospholipase C, which leads to the formation of IP 3 . Additionally, the formation of diacylglycerol (DAG) and protein kinase increases. In muscarinic synapses, both the site of binding to the mediator and the ion channel are not localized in the transmembrane protein itself. These receptors are directly coupled to the G-protein, which provides additional opportunities to influence the function of synapses. On the one hand, there are also competitive blockers for such receptors. In muscarinic synapses, this is, for example, atropine, an alkaloid found in plants of the nightshade family. On the other hand, compounds are known that themselves block the ion channel. They do not compete for binding sites and are so-called noncompetitive blockers. It is also known that some bacterial toxins, such as cholerotoxin or whooping cough toxin, have specific effects on the G-protein system at the level of the synaptic apparatus. Cholerotoxin prevents the hydrolysis of α-G s -GTP to α-G s -GDP and thereby increases the activity of adenylate cyclase. Pertusitoxin prevents the binding of GTP to the α-G i subunit of the G-protein and blocks the inhibitory effect of α-G i . This indirect action increases the concentration of cAMP in the cytosol. The transmission is very slow. The transmission time is in the range of 100 ms. Muscarinic synapses include postganglionic, parasympathetic, and CNS autoreceptors. Muscarinic receptors, derived from the axons of the Mounter cells of the nucleus basalis (Meyner cells), direct specific learning processes. In Alzheimer's disease (dementia), the number of Mounter cells in the nucleus decreases. Table 1.3 lists some of the substances that affect transmission at synapses.

Postsynaptic potential

Postsynaptic potential(PSP) is a temporary change in the potential of the postsynaptic membrane in response to a signal received from the presynaptic neuron. Distinguish:

  • excitatory postsynaptic potential (EPSP), which provides depolarization of the postsynaptic membrane, and
  • inhibitory postsynaptic potential (IPSP), which provides hyperpolarization of the postsynaptic membrane.

EPSP brings the cell potential closer to the threshold value and facilitates the occurrence of an action potential, while IPSP, on the contrary, makes it difficult to generate an action potential. Conventionally, the probability of triggering an action potential can be described as resting potential + the sum of all excitatory postsynaptic potentials - the sum of all inhibitory postsynaptic potentials > action potential triggering threshold.

Individual PSPs are usually small in amplitude and do not cause action potentials in the postsynaptic cell; however, unlike action potentials, they are gradual and can be summed up. There are two summation options:

  • temporal - combining the signals that came through one channel (when a new impulse arrives before the previous one fades)
  • spatial - superposition of EPSPs of neighboring synapses

The mechanism of occurrence of PSP

When an action potential arrives at the presynaptic terminal of a neuron, the presynaptic membrane is depolarized and voltage-gated calcium channels are activated. Calcium begins to enter the presynaptic ending and causes exocytosis of vesicles filled with a neurotransmitter. The neurotransmitter is released into the synaptic cleft and diffuses to the postsynaptic membrane. On the surface of the postsynaptic membrane, the neurotransmitter binds to specific protein receptors (ligand-gated ion channels) and causes them to open.

There are the following PSPs:

  1. Spontaneous and miniature PSPs
  2. End plate potential
  3. Caused PSP

Literature

  • Savelyev A. V. Modeling of functional neuronal self-organization under post-tetanic potentiation // Journal of Problems of the Evolution of Open Systems, Kazakhstan, Almaty, 2004, No. 1, p. 127-131.

see also

Links

Notes


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See what "Post-synaptic potential" is in other dictionaries:

    excitatory postsynaptic potential- - potential resulting from local depolarization of the postsynaptic membrane under the action of an excitatory mediator, EPSP (excitatory postsynaptic potential) ...

    Postsynaptic inhibitory potential- - potential resulting from local hyperpolarization of the postsynaptic membrane under the action of an inhibitory mediator, IPSP (inhibitory postsynaptic potential) ... Glossary of terms for the physiology of farm animals

    POSTSYNAPTIC POTENTIAL OF INHIBITION

    - (EPSP) potential resulting from local depolarization of the postsynaptic membrane under the action of an excitatory mediator ... Big Medical Dictionary

    - (TPSP) potential resulting from local hyperpolarization of the postsynaptic membrane under the action of an inhibitory mediator ... Big Medical Dictionary

    Postsynaptic potential (PSP)- - any change in the membrane potential of the postsynaptic neuron. PSP is caused by mediator substances secreted by presynaptic terminal plaques. Excitatory PSPs are states of depolarization that lower the threshold ... ...

    POST SYNAPTIC POTENTIAL (PSP)- In general, any change in the membrane potential of a postsynaptic neuron. PSPs are caused by mediator substances secreted by presynaptic terminal plaques. Post-synaptic excitatory potentials (PSEP) are ... ... Explanatory Dictionary of Psychology

    EXCITATIVE POSTSYNAPTIC POTENTIAL- See postsynaptic potential... Explanatory Dictionary of Psychology

    postsynaptic potential- short-term (from tens of milliseconds to a second) fluctuation of the membrane potential resulting from the action of the mediator on the postsynaptic membrane of the nerve cell. * * * The bioelectric potential arising under the influence of ... ... Encyclopedic Dictionary of Psychology and Pedagogy

    - (PKP) excitatory postsynaptic potential that occurs in the neuromuscular synapse during the transfer of excitation from the nerve to the muscle ... Big Medical Dictionary

In excitatory synapses of the nervous system, the mediator can be acetylcholine, norepinephrine, dopamine, serotonin, glugamic acid, substance P, as well as a large group of other substances that are, if not mediators in the direct sense, then at least modulators (changing efficiency) of synaptic transmission. Excitatory neurotransmitters cause the appearance on the postsynaptic membrane excitatory postsynaptic potential(VPSP). Its formation is due to the fact that the mediator-receptor complex activates Na-channels of the membrane (and probably also Ca-channels) and causes membrane depolarization due to the entry of sodium into the cell. Simultaneously, there is also a decrease in the release of K + ions from the cell. The amplitude of a single EPSP, however, is quite small, and simultaneous activation of several excitatory synapses is necessary to reduce the membrane charge to a critical level of depolarization.

EPSPs formed on the postsynaptic membrane of these synapses are capable of sum up, those. amplify each other, leading to an increase in the amplitude of the EPSP (spatial summation).

The amplitude of the EPSP increases and with an increase in the frequency of nerve impulses arriving at the synapse (time summation), which increases the number of mediator quanta released into the synaptic cleft.

The process of spontaneous regenerative depolarization occurs in a neuron, usually at the place where the axon cell leaves the body, in the so-called axon hillock, where the axon is not yet covered with myelin and the excitation threshold is the lowest. Thus, EPSPs that occur in different parts of the neuron membrane and on its dendrites propagate to the axon hillock, where they are summed up, depolarizing the membrane to a critical level and leading to the appearance of an action potential.

Inhibitory postsynaptic potential (IPSP) In inhibitory synapses, other, inhibitory, neurotransmitters usually act. Among them, the amino acid glycine (inhibitory synapses of the spinal cord), gamma-aminobutyric acid (GABA), an inhibitory mediator in brain neurons, are well studied. At the same time, the inhibitory synapse may have the same mediator as the excitatory synapse, but a different nature of the postsynaptic membrane receptors. Thus, for acetylcholine, biogenic amines, and amino acids, at least two types of receptors can exist on the postsynaptic membrane of different synapses, and, consequently, different mediator-receptor complexes can cause different reactions of chemosensitive receptor-gated channels. For an inhibitory effect, such a reaction may be the activation of potassium channels, which causes an increase in the release of potassium ions to the outside and hyperpolarization of the membrane. A similar effect in many inhibitory synapses is the activation of channels for chlorine, which increases its transport into the cell. The shift in the membrane potential that occurs during hyperpolarization is called inhibitory postsynaptic potential(TPSP). Figure 3.5 shows the distinguishing features of EPSP and IPSP. An increase in the frequency of nerve impulses arriving at the inhibitory synapse, as well as in excitatory synapses, causes an increase in the number of inhibitory transmitter quanta released into the synaptic cleft, which, accordingly, increases the amplitude of hyperpolarizing IPSP. However, IPSP is not capable of spreading across the membrane and exists only locally.


As a result of IPSP, the level of the membrane potential moves away from the critical level of depolarization, and excitation becomes either completely impossible, or excitation requires the summation of EPSPs that are much larger in amplitude, i.e. the presence of significantly higher excitation currents. With simultaneous activation of excitatory and inhibitory synapses, the amplitude of EPSP drops sharply, since the depolarizing flow of Na + ions is compensated by the simultaneous release of K + ions in some types of inhibitory synapses or the entry of SG ions into others, which is called bypass EPSP.

Under the influence of certain poisons, blockade of inhibitory synapses in the nervous system can occur, which causes uncontrolled excitation of numerous reflex apparatuses and manifests itself in the form of convulsions. This is how strychnine acts, which competitively binds the receptors of the postsynaptic membrane and does not allow them to interact with the inhibitory mediator. Tetanus toxin, which disrupts the release of the inhibitory neurotransmitter, also inhibits inhibitory synapses.

It is customary to distinguish between two types of inhibition in the nervous system: primary and secondary

Everything features of the spread of excitation in the central nervous system are explained by its neural structure: the presence of chemical synapses, multiple branching of axons of neurons, the presence of closed neural pathways. These features are as follows.

1. Irradiation (divergence) of excitation in the central nervous system. It is explained by the branching of the axons of neurons, their ability to establish numerous connections with other neurons, the presence of intercalary neurons, the axons of which also branch (Fig. 4.4, a).

Irradiation of excitation can be observed in an experiment on a spinal frog, when a weak irritation causes flexion of one limb, and a strong one causes energetic movements of all the limbs and even the trunk. Divergence expands the scope of each neuron. One neuron, sending impulses to the cerebral cortex, can participate in the excitation of up to 5000 neurons.

Rice. 4.4. Divergence of afferent dorsal roots to spinal neurons, the axons of which, in turn, branch, forming numerous collaterals (c), and convergence of efferent pathways from different parts of the CNS to the α-motoneuron of the spinal cord (6)

1. Convergence of excitation (the principle of a common final path) - the convergence of excitation of various origins along several paths to the same neuron or neuronal pool (the principle of the Sherrington funnel). The convergence of excitation is explained by the presence of many axon collaterals, intercalary neurons, and also by the fact that there are several times more afferent pathways than efferent neurons. Up to 10,000 synapses can be located on one CNS neuron. The phenomenon of convergence of excitation in the CNS is widespread. An example is the convergence of excitation on the spinal motor neuron. So, primary afferent fibers (Fig. 4.4, b), as well as various descending paths of many overlying centers of the brain stem and other parts of the central nervous system, approach the same spinal motor neuron. The phenomenon of convergence is very important: it provides, for example, the participation of one motor neuron in several different reactions. The motor neuron innervating the muscles of the pharynx is involved in the reflexes of swallowing, coughing, sucking, sneezing and breathing, forming a common final path for numerous reflex arcs. On fig. 4.4, I show two afferent fibers, each of which gives collaterals to 4 neurons in such a way that 3 of their total number of 5 neurons form connections with both afferent fibers. On each of these 3 neurons, two afferent fibers converge.

Many axon collaterals, up to 10,000–20,000, can converge on one motor neuron, so the generation of AP at each moment depends on the total amount of excitatory and inhibitory synaptic influences. PD arise only if excitatory influences predominate. Convergence can facilitate the process of excitation on common neurons as a result of spatial summation of subthreshold EPSPs or block it due to the predominance of inhibitory influences (see Section 4.8).

3. Circulation of excitation through closed neural circuits. It can last minutes and even hours (Fig. 4.5).

Rice. 4.5. Excitation circulation in closed neural circuits according to Lorento de No (a) and according to I.S. Beritov (b). 1,2,3 - excitatory neurons

Excitation circulation is one of the causes of the aftereffect phenomenon, which will be discussed further (see section 4.7). It is believed that the circulation of excitation in closed neural circuits is the most likely mechanism for the phenomenon of short-term memory (see section 6.6). Circulation of excitation is possible in a chain of neurons and within a single neuron as a result of the contacts of the branches of its axon with its own dendrites and body.

4. Unilateral distribution of excitation in neural circuits, reflex arcs. The spread of excitation from the axon of one neuron to the body or dendrites of another neuron, but not vice versa, is explained by the properties of chemical synapses that conduct excitation in only one direction (see Section 4.3.3).

5. The slow propagation of excitation in the CNS compared to its propagation along the nerve fiber is explained by the presence of many chemical synapses along the pathways of the propagation of excitation. The time for conducting excitation through the synapse is spent on the release of the mediator into the synaptic cleft, its propagation to the postsynaptic membrane, the occurrence of EPSP, and, finally, AP. The total delay in the transmission of excitation in the synapse reaches approximately 2 ms. The more synapses in the neuronal chain, the lower the overall rate of propagation of excitation along it. According to the latent time of the reflex, more precisely, according to the central time of the reflex, it is possible to roughly calculate the number of neurons of a particular reflex arc.

6. The spread of excitation in the CNS is easily blocked by certain pharmacological drugs, which is widely used in clinical practice. Under physiological conditions, restrictions on the spread of excitation through the CNS are associated with the activation of neurophysiological mechanisms of neuronal inhibition.

The considered features of the propagation of excitation make it possible to approach the understanding of the properties of the nerve centers.

4. MODERN CONCEPTS ON THE FORMS AND MECHANISMS OF INDERATION IN THE CNS. FUNCTIONAL SIGNIFICANCE OF VARIOUS FORMS OF BRAKING.

Braking in the central nervous system, it is the process of weakening or stopping the transmission of nerve impulses. Inhibition limits the spread of excitation (irradiation) and allows for fine regulation of the activity of individual neurons and the transmission of signals between them. The most common inhibitory neurons are the interneurons. It is thanks to the interaction of the processes of excitation and inhibition in the central nervous system that the activities of individual body systems are combined into a single whole (integration) and the coordination and coordination of their activities. For example, concentration of attention can be seen as a weakening of irradiation and an increase in induction. This process improves with age. The significance of inhibition also lies in the fact that from all the sense organs, from all the receptors to the brain, there is a continuous flow of signals, but the brain does not react to everything, but only to the most significant at the moment. Braking allows you to more accurately coordinate the work of different organs and systems of the body. With the help of presynaptic inhibition, the flow of certain types of nerve impulses to the nerve centers is limited. Postsynaptic inhibition weakens reflex reactions that are currently unnecessary or insignificant. It underlies, for example, the coordination of muscle work.

Distinguish between primary and secondary inhibition. Primary braking develops initially. without prior excitation and manifests itself in hyperpolarization of the neuronal membrane under the action of inhibitory neurotransmitters. For example, reciprocal inhibition under the action of inhibitory neurotransmitters. Primary inhibition includes presynaptic and postsynaptic inhibition, while secondary inhibition includes pessimal and inhibition following excitation. Secondary braking arises without the participation of special inhibitory structures, as a result of excessive activation of excitatory neurons (Vvedensky inhibition). It plays a protective role. Secondary inhibition is expressed in persistent depolarization of neuronal membranes, exceeding the critical level and causing inactivation of sodium channels. Central inhibition (I.M. Sechenov) is inhibition caused by excitation and manifested in the suppression of another excitation.

Braking classification:

I. According to the localization of the place of application in the synapse:

1 – presynaptic inhibition- observed in axo-axonal synapses, blocking the spread of excitation along the axon (in the structures of the brain stem, in the spinal cord). In the contact area, an inhibitory mediator (GABA) is released, causing hyperpolarization, which disrupts the conduction of the excitation wave through this area.

2 - postsynaptic inhibition- the main type of inhibition, develops on the postsynaptic membrane of axosomatic and axodendrial synapses under the influence of released GABA or glycine. The action of the mediator causes the effect of hyperpolarization in the form of IPSP in the postsynaptic membrane, which leads to a slowdown or complete cessation of AP generation.

II. By effects in neural circuits and reflex arcs:

1 – reciprocal inhibition - carried out to coordinate the activity of muscles opposite in function (Sherrington). For example, a signal from the muscle spindle comes from an afferent neuron to the spinal cord, where it switches to the flexor α motor neuron and simultaneously to an inhibitory neuron that inhibits the activity of the extensor α motor neuron.

2 – return braking- is carried out to limit the excessive excitation of the neuron. For example, an α-motor neuron sends an axon to the corresponding muscle fibers. Along the way, a collateral departs from the axon, which returns to the CNS - it ends on an inhibitory neuron (Renshaw cell) and activates it. The inhibitory neuron causes inhibition of the α-motor neuron, which launched this entire chain, that is, the α-motor neuron inhibits itself through the system of the inhibitory neuron.

3 - lateral inhibition(return option). Example: a photoreceptor activates a bipolar cell and at the same time a nearby inhibitory neuron that blocks the conduction of excitation from a neighboring photoreceptor to a ganglion cell (“inhibition of information”.

III. According to the chemical nature of the neurotransmitter:

1 - GABAergic,

2 - glycinergic,

3 - mixed.

IV. Classification of types of braking according to I.P. Pavlov(Table 1)

Table 1 - Types of braking (according to I.P. Pavlov)

Braking type Type of braking Characteristic biological significance
Unconditional braking External Distraction due to unexpected new stimuli Change of dominant, switching to the collection of new information
Beyond The result of fatigue "Protective", protection of the nervous system from damage
Conditional fading Decreased response to non-reinforced conditioned stimulus Refusal of ineffective behavioral programs, forgetting unused programs
Differential Cessation of response to a similar but unreinforced stimulus Fine discrimination of similar sensory signals
Conditional brake When presented with a stimulus signaling that there will be no reinforcement following the conditioned stimulus "Prohibitions", stopping current activities under certain conditions
delayed During the pause between the prearranged signal and the delayed reinforcement "Expectation"

Inhibitory postsynaptic potential - hyperpolarization of the postsynaptic membrane in retarded synapses. According to the temporal course, the inhibitory postsynaptic potential is a mirror image of the excitatory postsynaptic potential with a rise and fall time of 1-2 and 10-12 ms, respectively. The shift in the conductivity of the postsynaptic membrane also lasts about 1–2 ms.

Under the action of inhibitory neurotransmitters in the postsynaptic membrane, channels for chloride ions open, as a result of which chloride ions enter the cell, the negative charge on the inner side of the membrane increases and hyperpolarization of the membrane occurs - an inhibitory postsynaptic potential (IPSP) is formed, which hinders the formation of AP.

27. Summation of vpsp.

Summation - the phenomenon of summation of the depolarizing effects of several excitatory postsynaptic potentials, each of which cannot cause depolarization of the threshold value necessary for the occurrence of an action potential.

Distinguish between spatial summation and temporal summation.

Spatial summation- summation as a result of the action of several excitatory postsynaptic potentials that arose simultaneously in different synapses of the same neuron.

Time summation- often repeated release of a mediator from synaptic vesicles of the same synaptic plaque under the influence of an intense stimulus that causes separate excitatory postsynaptic potentials that follow so often one after another in time that their effects are summed up and cause an action potential in the postsynaptic neuron.

28. Types of inhibition in the central nervous system

Inhibition in the CNS(I.M. Sechenov) is the process of weakening or stopping the transmission of nerve impulses.

Braking classification:

I. By neurophysiological mechanisms:

1 – presynaptic inhibition- observed in axo-axonal synapses, blocking the spread of excitation along the axon (in the structures of the brain stem, in the spinal cord). In the contact area, an inhibitory mediator (GABA) is released, causing hyperpolarization, which disrupts the conduction of the excitation wave through this area.

2 – postsynaptic inhibition- the main type of inhibition, develops on the postsynaptic membrane of axosomatic and axodendrial synapses under the influence of released GABA or glycine. The action of the mediator causes the effect of hyperpolarization in the form of IPSP in the postsynaptic membrane, which leads to a slowdown or complete cessation of AP generation.

3 - Pessimal braking- 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.

4 -Inhibition followed by 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.

II. By effects in neural circuits and reflex arcs:

1 – reciprocal inhibition- carried out to coordinate the activity of muscles opposite in function (Sherrington). For example, a signal from the muscle spindle comes from an afferent neuron to the spinal cord, where it switches to the flexor α motor neuron and simultaneously to an inhibitory neuron that inhibits the activity of the extensor α motor neuron.

2 - reverse braking- is carried out to limit the excessive excitation of the neuron. For example, an α-motor neuron sends an axon to the corresponding muscle fibers. Along the way, a collateral departs from the axon, which returns to the CNS - it ends on an inhibitory neuron (Renshaw cell) and activates it. The inhibitory neuron causes inhibition of the α-motor neuron, which launched this entire chain, that is, the α-motor neuron inhibits itself through the system of the inhibitory neuron.

3 – lateral inhibition(return option). Example: a photoreceptor activates a bipolar cell and at the same time a nearby inhibitory neuron that blocks the conduction of excitation from a neighboring photoreceptor to a ganglion cell (“inhibition of information”.

III. According to the chemical nature of the neurotransmitter:

1 - GABAergic,

2 - glycinergic,

3 - mixed.

By biological significance: coordination and protective.

By localization: spilled and limited.

By origin: congenital and acquired.

The action of the mediator on the postsynaptic membrane of a chemical synapse leads to the appearance of a postsynaptic potential in it. Postsynaptic potentials can be of two types: depolarizing (excitatory) and hyperpolarizing (inhibitory) (Fig. 5.5).

Excitatory postsynaptic potentials(EPSP) are due to the total incoming current of positive charges into the cell. This current may result from increased membrane conductivity for sodium, potassium, and possibly other ions (eg, calcium).

Rice. 5.5.

but - activation of only the excitatory synapse; b - activation of only the inhibitory synapse; in - activation of both excitatory and inhibitory synapses

As a result, the membrane potential shifts towards zero (becomes less negative). In fact, the value of VSI depends on which ions have moved through the membrane and what is the ratio of permeabilities for these ions. The movements of various ions occur simultaneously, and their intensity depends on the amount of released mediator.

Thus, postsynaptic potentials are gradual reactions (their amplitude depends on the amount of mediator released or the strength of the stimulus). In this they differ from the action potential, which obeys the all-or-nothing law.

VESI is necessary for the generation of a nerve impulse (NIR). This happens if the VSI reaches the threshold value. After that, the processes become irreversible, and PD occurs. So, excitation in cells can occur for various reasons (Fig. 5.6), but in any case, for its development, a change in the permeability of the membrane for ions must occur. Braking develops according to similar mechanisms.


Rice. 5.6.

If channels open in the membrane that provide a total outgoing current of positive charges (potassium ions) or an incoming current of negative charges (chlorine ions), then the cell develops inhibitory postsynaptic potential(TPSP). Such currents will lead to the retention of the membrane potential at the level of the resting potential or to some hyperpolarization.

Direct chemical synaptic inhibition occurs when channels for negatively charged chloride ions are activated. Stimulation of inhibitory inputs causes a slight hyperpolarization of the cell - inhibitory postsynaptic potential. As mediators causing TGTSP, glycine and gamma-aminobutyric acid (GABA) were found; their receptors are connected to channels for chlorine, and when these mediators interact with their receptors, chloride ions move into the cell and the membrane potential increases (up to -90 or -100 mV). This process is called postsynaptic inhibition.

However, in some cases, inhibition cannot be explained only in terms of postsynaptic changes in conduction. J. Eccles and his collaborators discovered an additional mechanism of inhibition in the spinal cord of mammals: presynaptic inhibition. As a result of presynaptic inhibition, there is a decrease in the release of the mediator from excitatory endings. During presynaitic inhibition, inhibitory axons establish synaptic contact with the endings of excitatory axons. GABA is the most common mediator of presynaptic inhibition. As a result of the action of GABA on the presynaptic ending, there is also a significant increase in the conductivity for chlorine and, as a result, a decrease in the AP amplitude in the presynaptic ending.

The functional significance of these two types of inhibition in the CNS differs greatly. Postsynaptic inhibition reduces the excitability of the entire cell as a whole, making it less sensitive to all excitatory inputs. Presynaptic inhibition is much more specific and selective. It is directed to a particular input, allowing the cell to integrate information from other inputs.