When Na + ions enter the cell, the excitability of the postsynaptic membrane increases, it depolarizes. Therefore, the receptor that opens the sodium channel transmits the excitatory effect. The postsynaptic potential that occurs in this case is called excitatory postsynaptic potential - EPSP(see fig. 16, pos. A).
Inhibitory postsynaptic potential - IPSP
Other sites on the receptors, which, for example, bind gamma-aminobutyric acid (GABA), open channels in the postsynaptic membrane for the entry of Cl- ions into the cell and reduce the excitability of the postsynaptic membrane, it hyperpolarized. This means that the receptor that opens the chloride channel represents an inhibitory effect. And the postsynaptic potential that occurs in this case is called inhibitory postsynaptic potential - IPSP(see fig. 16, pos. B).
Summation
Consider another mechanism of integration at the level of one neuron, which is called summation.
Summation(lat. summation- addition) - fusion of local responses to subthreshold stimuli. Remember! Under the action of a single subthreshold stimulus, AP does not occur.
There are two types of summation:
1) temporary (consecutive);
2) spatial (simultaneous).
The mechanism of summation in the CNS was first described by I. M. Sechenov (1868), who observed, under certain conditions of rhythmic stimulation, a delay in the appearance and subsequent intensification of reflex reactions.
Time summation is the result of the addition of postsynaptic local responses, which are caused by several successive afferent stimuli quickly following each other (Fig. 17).
A prerequisite for this type of summation are short intervals between incoming stimuli. The stimuli should come at such an interval that the subsequent local responses caused by them could be summed up with the previous ones that did not have time to “fade out”. Thus, temporal summation at the synapse allows filtering out weak signals coming to the neuron.
Let us examine in detail the mechanism of the occurrence of time summation. In response to a single afferent stimulus going from a neuron to another neuron, 1 neurotransmitter quantum is released in the presynaptic part of the synapse. In this case, a subthreshold potential (local response) of 0.1-0.2 mV, which is insufficient for generating AP, usually appears on the postsynaptic membrane of the neuron. In order for the magnitude of the local response to reach a critical level - the threshold for the occurrence of AP, it must decrease by about 10 mV. This requires the summation of many subthreshold local responses on the postsynaptic cell membrane. Summation is the cumulative result of the action on the neuron of input sensory stimuli. The summation of postsynaptic potentials occurs at the axon hillock of the neuron, where the propagating action potential occurs.
The opening of nonspecific channels for cations during the interaction of ACh with the ACh receptor leads to a strong inward current of Na+ ions and a weaker outward current of K+ ions on the postsynaptic membrane. Ultimately, more positive charges flow into the cell. There is a local depolarization of the membrane, which is called the excitatory postsynaptic potential (EPSP).
Interacting with the receptor, ACh molecules open nonspecific ion channels in the postsynaptic cell membrane so that their ability to conduct for monovalent cations increases. Which cations pass through the channels depends on electrochemical gradients. The equilibrium potential for sodium is +55 mV, and the potential of the membrane of the postsynaptic cell lies in the range from -60 to -80 mV. Thus, there is a strong driving force for sodium, and its ions rush into the cell and depolarize its membrane (Fig. 21.5, Fig. 21.7). On the other hand, the channel is also traversable for K+ ions, for which an insignificant electrochemical gradient is preserved, directed from the intracellular region to the extracellular medium. Since the equilibrium potential of K + ions is approximately -90 mV, they also pass through the postsynaptic membrane, thereby slightly counteracting the depolarization due to the incoming current of Na + ions. The operation of these channels leads to a basic inward current of positive ions and, consequently, to the depolarization of the postsynaptic membrane (EPSP). At the end plate of the neuromuscular junction, the EPSP is also called the end plate potential (EPP). Since the involved ion currents depend on the difference between the equilibrium potential and the membrane potential, then at a reduced resting potential of the membrane, the current of Na + ions weakens, and the current of K + ions increases, therefore, the amplitude of the EPSP decreases.
The ionic currents involved in the generation of EPSPs behave differently than the Na+ and K+ currents during action potential generation. The reason is that other ion channels with different properties are involved in this mechanism. While voltage-gated ion channels are activated at an action potential and subsequent channels open with increasing depolarization, so that the depolarization process reinforces itself, the conductance of transmitter-gated (ligand-gated) channels depends only on the number of transmitter molecules bound to the receptor molecules (resulting in the opening of transmitter-gated channels). ion channels), and, consequently, on the number of open ion 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.
First of all, in the synapse zone, the locally formed EPSP passively electrotonically propagates throughout the entire postsynaptic cell membrane. This distribution is not subject to the all-or-nothing law. If a large number of synapses are excited simultaneously or almost simultaneously, then the so-called summation phenomenon occurs, which manifests itself in 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 value in the area of the postsynaptic membrane (10 mV or more), then voltage-controlled Na + channels open at lightning speed on the axon hillock of the nerve cell and it generates an action potential that is conducted 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, about 0.3 ms passes, so that with abundant release of the transmitter, the postsynaptic potential can appear as early as 0.5–0.6 ms after the action potential that has arrived in the presynaptic region.
In general terms, the time of "synaptic delay", meaning the necessary time between the occurrence of the pre- and postsynaptic action potential, always depends on the type of synapse.
Generation of action potentials occurs in the interception of Ranvier of myelinated fibers closest to the receptors or in the part of the membrane of the unmyelinated fiber closest to the receptors. The minimum strength of an adequate stimulus sufficient to generate action potentials in a primary sensory neuron is defined as its absolute threshold. The minimum increase in the strength of the stimulus, accompanied by a significant change in the response of the sensory neuron, is the differential threshold of its sensitivity.
Information about the strength of the stimulus acting on the receptors is encoded in two ways: the frequency of action potentials that occur in the sensory neuron (frequency coding), and the number of sensory neurons fired in response to the stimulus. With an increase in the strength of the stimulus acting on the receptors, the amplitude of the receptor potential increases, which, as a rule, is accompanied by an increase in the frequency of action potentials in the first-order sensory neuron. The wider the available frequency range of action potentials in sensory neurons, the greater the number of intermediate values of the strength of the stimulus is able to distinguish the sensory system. Primary sensory neurons of the same modality differ in the threshold of excitation, therefore, under the action of weak stimuli, only the most sensitive neurons are excited, but with an increase in the strength of the stimulus, less sensitive neurons with a higher threshold of irritation also respond to it. The more primary sensory neurons are simultaneously excited, the stronger will be their joint action on the common second-order neuron, which will ultimately affect the subjective assessment of the intensity of the acting stimulus.
The duration of sensation depends on the real time between the beginning and end of the impact on the receptors, as well as on their ability to reduce or even stop the generation of nerve impulses during prolonged action of an adequate stimulus. With prolonged action of the stimulus, the sensitivity threshold of receptors to it can increase, which is defined as receptor adaptation. Adaptation mechanisms are not the same in receptors of different modalities; among them, quickly adapting (for example, skin tactile receptors) and slowly adapting receptors (for example, muscle and tendon proprioceptors) are distinguished. Rapidly adapting receptors are more strongly excited in response to a rapid increase in stimulus intensity (phasic response), and their rapid adaptation facilitates the release of perception from biologically insignificant information (for example, contact between skin and clothing). Excitation of slowly adapting receptors does not depend much on the rate of change of the stimulus and persists during its long-term action (tonic response), therefore, for example, slow adaptation of proprioceptors allows a person to receive the information he needs to maintain a posture for the entire necessary time.
There are sensory neurons that spontaneously generate action potentials, i.e., in the absence of stimulation (for example, sensory neurons of the vestibular system), such activity is called background. The frequency of nerve impulses in these neurons can increase or decrease depending on the intensity of the stimulus acting on the secondary receptors, in addition, it can be determined by the direction in which the sensitive hairs of the mechanoreceptors deviate. For example, the deviation of hairs of secondary mechanoreceptors in one direction is accompanied by an increase in the background activity of the sensory neuron to which they belong, and in the opposite direction, by a decrease in its background activity. This method of reception makes it possible to obtain information both about the intensity of the stimulus and about the direction in which it acts.
4 Inhibition in the CNS
Inhibition in the central nervous system was first discovered in 1862 by I. M. Sechenov in the experiment of stimulating the brain of a frog at the level of the visual halls, where a narrow strip of gray matter of the brain stem is located - a homologue of the hypotuberous region of the brain of higher animals and humans. The imposition of a sodium chloride crystal on a cross section of the brain in the region of the visual halls causes an increase in the time (inhibition) of the spinal motor reflex caused by immersing the frog's foot in a weak acid solution. Somewhat later, I. M. Sechenov found that with simultaneous stimulation of two afferent nerves that carry excitation to the spinal cord, a stronger irritation inhibits the reflex to a weaker one, for example, pinching the frog’s right foot with tweezers causes an increase in the time of the acid reflex (up to its complete prolapse) of the left paw.
In the experiments of I. M. Sechenov, inhibition of some nerve centers occurs as a result of excitation of the centers of others, as a phenomenon that accompanies excitation in the central nervous system. The initial assumption of I. M. Sechenov about the presence of specifically inhibitory nerve centers has disappeared, since it turned out (in the experiments of his student V. V. Pashutin, one of the founders of pathological physiology in Russia), that when the visual halls of the frog are stimulated, in a number of experiments, there is no slowdown spinal motor reflexes, and their acceleration. The mechanisms of the occurrence of inhibition in the experiments of I. M. Sechenov are different. Irritation in the area of the visual halls - the center of the autonomic nervous system - causes Sechenov's inhibition only with the preserved sympathetic chain and therefore is considered as the result of trophic shifts transmitted along the sympathetic nerve fibers to the spinal cord (A. V. Tonkikh, laboratory L. A. Orbeli). The inhibition of the acid motor reflex, which occurs as a result of simultaneous mechanical stimulation of the skin receptors of the other limb, is the result of induction relationships that cause the suppression of competing nerve centers.
Braking- a special nervous process, which is caused by excitation and is outwardly manifested by the inhibition of another excitation. It is able to actively spread by the nerve cell and its processes. The theory of central inhibition was founded by IM Sechenov (1863), who noticed that the frog's bending reflex is inhibited by chemical stimulation of the midbrain. Inhibition plays an important role in the activity of the central nervous system, namely: in the coordination of reflexes; in human and animal behavior; in the regulation of the activity of internal organs and systems; in the implementation of the protective function of nerve cells.
Types of inhibition in the CNS
Central inhibition is distributed according to localization into pre- and postsynaptic;
by the nature of polarization (membrane charge) - on hyper- and depolarization; according to the structure of inhibitory neural circuits - into reciprocal, or connected, reverse and lateral.
presynaptic inhibition, as the name indicates, is localized in presynaptic elements and is associated with inhibition of the conduction of nerve impulses in axonal (presynaptic) endings. The histological substrate of such inhibition is axonal synapses. An insertion inhibitory axon approaches the excitatory axon and releases the inhibitory neurotransmitter GABA. This mediator acts on the postsynaptic membrane, which is the membrane of the excitatory axon, and causes depolarization in it. The resulting depolarization inhibits the entry of Ca2 + from the synaptic cleft into the conclusion of the excitatory axon and thus leads to a decrease in the release of the excitatory mediator into the synaptic cleft, inhibition of the reaction. Presynaptic inhibition reaches a maximum after 15-20 ms and lasts about 150 ms, that is, much longer than postsynaptic inhibition. Presynaptic inhibition is blocked by convulsive poisons - biculin and picrotoxin, which are competitive GABA antagonists.
Postsynaptic inhibition(GPSP) is caused by the release of an inhibitory mediator by the presynaptic ending of the axon, which reduces or inhibits the excitability of the membranes of the soma and dendrites of the nerve cell with which it contacts. It is associated with the existence of inhibitory neurons, the axons of which form on the soma and dendrites of nerve ending cells, releasing inhibitory mediators - GABA and glycine. Under the influence of these mediators, inhibition of excitatory neurons occurs. Examples of inhibitory neurons are Renshaw cells in the spinal cord, pear-shaped neurons (Purkinje cells of the cerebellum), stellate cells of the cerebral cortex, brain, etc.
A study by P. G. Kostyuk (1977) proved that postsynaptic inhibition is associated with primary hyperpolarization of the membrane of the soma of the neuron, which is based on an increase in the permeability of the postsynaptic membrane for K +. As a result of hyperpolarization, the level of the membrane potential moves away from the critical (threshold) level. That is, its increase occurs - hyperpolarization. This leads to the inhibition of the neuron. This type of inhibition is called hyperpolarization.
The amplitude and polarity of the HPSP depend on the initial level of the membrane potential of the neuron itself. The mechanism of this phenomenon is associated with Cl + . With the onset of IPSP development, Cl - enters the cell. When there is more of it inside the cell than outside, glycine conforms to the membrane and Cl + exits the cell through its open holes. It reduces the number of negative charges, depolarization develops. This type of inhibition is called depolarization.
Postsynaptic inhibition is local. It develops gradually, capable of summation, leaving no refractoriness behind. It is a more responsive, well-targeted and versatile braking mechanism. At its core, this is "central inhibition", which was described at the time by Ch. S. Sherrington (1906).
Depending on the structure of the inhibitory neuronal chain, the following forms of postsynaptic inhibition are distinguished: reciprocal, reverse and lateral, which is actually a kind of reverse.
Reciprocal (combined) inhibition characterized the fact that in the case when, for example, the motor neurons of the flexor muscles are excited during activation of the afferents, the motor neurons of the extensor muscles acting on the same joint are simultaneously (on this side) inhibited. This happens because the afferents from the muscle spindles form excitatory synapses on the motoneurons of the agonist muscles, and through the intervening inhibitory neuron, inhibitory synapses on the motoneurons of the antagonist muscles. From a physiological point of view, such inhibition is very beneficial, since it facilitates the movement of the joint “automatically”, without additional voluntary or involuntary control.
Reverse braking . In this case, one or more collaterals depart from the axons of the motor neuron, which are directed to the intercalated inhibitory neurons, for example, Renshaw cells. In turn, Renshaw cells form inhibitory synapses on motor neurons. In the case of excitation of the motor neuron, Renshaw cells are also activated, as a result of which hyperpolarization of the motor neuron membrane occurs and its activity is inhibited. The more the motor neuron is excited, the greater the tangible inhibitory effects through Renshaw cells. Thus, reverse postsynaptic inhibition functions on the principle of negative feedback. There is an assumption that this type of inhibition is required for self-regulation of excitation of neurons, as well as to prevent their overexcitation and convulsive reactions.
Lateral inhibition. The inhibitory chain of neurons is characterized by the fact that inhibitory neurons affect not only the inflamed cell, but also neighboring neurons, in which excitation is weak or completely absent. Such inhibition is called lateral, since the site of inhibition that is formed is contained laterally (laterally) from the excited neuron. It plays a particularly important role in sensory systems, creating the phenomenon of contrast.
Postsynaptic inhibition predominantly easily removed with the introduction of strychnine, which competes with the inhibitory mediator (glycine) on the postsynaptic membrane. Tetanus toxin also inhibits postsynaptic inhibition by interfering with neurotransmitter release from inhibitory presynaptic endings. Therefore, the introduction of strychnine or tetanus toxin is accompanied by convulsions that occur as a result of a sharp increase in the excitation process in the central nervous system, in particular, motor neurons.
In connection with the discovery of the ionic mechanisms of postsynaptic inhibition, it became possible to explain the mechanism of action of Br. Sodium bromide in optimal doses is widely used in clinical practice as a sedative (sedative) agent. It has been proven that this effect of sodium bromide is associated with increased postsynaptic inhibition in the CNS.
The role of various types of central inhibition
The main role of central inhibition is to provide, in interaction with central excitation, the possibility of analyzing and synthesizing nerve signals in the central nervous system, and, consequently, the possibility of coordinating all body functions with each other and with the environment. This role of central inhibition is called coordination. Some types of central inhibition perform not only a coordinating, but also a protective (guard) role. It is assumed that the main coordinating role of presynaptic inhibition is the suppression in the CNS by insignificant afferent signals. Due to direct postsynaptic inhibition, the activity of antagonistic centers is coordinated. Reverse inhibition, limiting the maximum possible frequency of discharges of motoneurons of the spinal cord, performs both a coordinating role (coordinates the maximum frequency of motoneuron discharges with the rate of contraction of the muscle fibers that they innervate) and protective (prevents the excitation of motoneurons). In mammals, this type of inhibition is distributed mainly in the spinal afferent systems. In the higher parts of the brain, namely in the cortex of the cerebrum, postsynaptic inhibition dominates.
Presynaptic inhibition (Latin prae - ahead of something + Greek sunapsis contact, connection) is a special case of synaptic inhibitory processes, manifested in the suppression of neuron activity as a result of a decrease in the effectiveness of excitatory synapses even at the presynaptic link by inhibiting the process of mediator release by excitatory nerve endings . In this case, the properties of the postsynaptic membrane do not undergo any changes.
6Presynaptic 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. 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.
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.
A characteristic feature of presynaptic depolarization is slow development and long duration (several hundred milliseconds), even after a single afferent impulse.
What is the functional significance of presynaptic inhibition? Due to it, the impact is carried out not only on the own reflex apparatus of the spinal cord, but also on the synaptic switching of a number of tracts ascending through the brain. It is also known about the descending presynaptic inhibition of the primary afferent fibers of the Aa group and skin afferents. In this case, presynaptic inhibition is obviously the first "tier" of active restriction of information coming from outside. In the CNS, especially in the spinal cord, presynaptic inhibition often acts as a kind of negative feedback that limits afferent impulses during strong (for example, pathological) stimuli and thus partly performs a protective function in relation to the spinal and higher located centers.
The functional properties of synapses are not constant. Under certain conditions, the effectiveness of their activities may increase or decrease. Usually, at high frequencies of stimulation (several hundred per 1 s), synaptic transmission is facilitated within a few seconds or even minutes. This phenomenon is called synaptic potentiation. Such synaptic potentiation can also be observed after the end of tetanic stimulation. Then it will be called post-tetanic potentiation (PTP). At the heart of PTP (long-term increase in the efficiency of communication between neurons), it is likely that there are changes in the functionality of the presynaptic fiber, namely its hyperpolarization. In turn, this is accompanied by an increase in the release of the neurotransmitter into the synaptic cleft and the appearance of an increased EPSP in the postsynaptic structure. There are also data on structural changes in PTP (swelling and growth of presynaptic endings, narrowing of the synaptic gap, etc.).
PTP is much better expressed in the higher parts of the CNS (for example, in the hippocampus, pyramidal neurons of the cerebral cortex) compared to spinal neurons. Along with PTP, post-activation depression may occur in the synaptic apparatus, which is expressed by a decrease in the amplitude of EPSP. This depression is associated by many researchers with a weakening of the sensitivity to the action of the neurotransmitter (desensitization) of the postsynaptic membrane or a different ratio of costs and mobilization of the mediator.
The plasticity of synaptic processes, in particular, PTP, may be associated with the formation of new interneuronal connections in the CNS and their fixation, i.e. mechanisms of learning and memory. At the same time, it should be recognized that the plastic properties of central synapses have not yet been sufficiently studied.
An action potential arriving at the presynaptic terminal causes the neurotransmitter to be released into the synaptic cleft. When the neurotransmitter reaches the postsynaptic terminal, it binds to receptors on the postsynaptic membrane, a miniature excitatory postsynaptic potential(EPSP) - about 0.05 mV. Such a local potential is not sufficient to change the state of the cell. However, many excitatory postsynaptic potentials arise at once; they, unlike the action potential, are summed up in order to reach a critical level of depolarization. When the AC is reached, the generation of the action potential begins. Excitatory postsynaptic potentials can be summed up only if they occur simultaneously, synchronously (in this case, the resting potential does not have time to recover and the membrane depolarization increases).
Sometimes there are spontaneous releases of the mediator from the presynaptic ending due to random collisions of vesicles and the membrane. However, the action potential does not arise in this case due to the small magnitude of the excitatory postsynaptic potential.
In addition to the processes of excitation on the membrane, reverse processes of inhibition can also occur. Inhibition in the NS is not a passive process of lack of activity, but an active blocking activity. In the case of inhibition, not excitatory postsynaptic potentials arise on the membrane, but inhibitory postsynaptic potentials, TPSP. When inhibitory postsynaptic potentials occur, membrane hyperpolarization occurs. IPSP does not cause a decrease, but an increase in the potential difference across the membrane, which prevents the formation of an action potential. Converging currents are formed on the membrane, that is, hyperpolarization "flows" to the axon from all places where the inhibitory effect has occurred. IPSP occurs when anions enter the cell, which easily pass through the channels. Most often it is Cl-.
Previously, it was believed that different mediators were responsible for the occurrence of EPSP and IPSP. The main inhibitory mediators include GABA (in the cortical and subcortical regions) and glycine (in the periphery and SM). However, it is now believed that it is not the mediator itself that is responsible for the generation of EPSP or IPSP (GABA can also cause an activating effect). The mediator, getting on the postsynaptic membrane, binds to the receptor, which, in turn, affects a special G-protein that activates the ion channel proteins. The G protein binds to a messenger that influences the functioning of the ion channel. Depending on the activity of this G-protein, either anion or cation channels are opened, and, accordingly, either EPSP or IPSP is generated.
Properties of postsynaptic potential:
- Occur only specifically in the place where the effect of the mediator occurred. Usually, it is a dendrite or soma.
- Value = 0.05 mV
- Unlike PD, they are cumulative.
The mediator located in the vesicles is released into the synaptic cleft by exocytosis. (bubbles approach the membrane, merge with it and burst, releasing the neurotransmitter). Its release occurs in small portions - quanta. Each quantum contains from 1,000 to 10,000 neurotransmitter molecules. A small number of quanta come out of the ending and are at rest. When the nerve impulse, i.e. AP reaches the presynaptic end, depolarization of its presynaptic membrane occurs. Its calcium channels open and calcium ions enter the synaptic plaque. The release of a large number of neurotransmitter quanta begins. Transmitter molecules diffuse through the synaptic cleft to the postsynaptic membrane and interact with its chemoreceptors. As a result of the formation of mediator-receptor complexes, the synthesis of so-called secondary messengers begins in the subsynaptic membrane. In particular cAMP. These mediators activate ion channels in the postsynaptic membrane. Therefore, such channels are called chemodependent or receptor-gated. Those. they open under the action of PAS on chemoreceptors. As a result of the opening of the channels, the potential of the subsynaptic membrane changes. This change is called postsynaptic potential.
In the CNS, excitatory are choline-, adren-, dopamine-, serotonergic synapses and some others. When their mediators interact with the corresponding receptors, chemodependent sodium channels open. Sodium ions enter the cell through the subsynaptic membrane. There is its local or spreading depolarization. This depolarization is called an excitatory postsynaptic potential (EPSP).
Inhibitory are glycine and GABAergic synapses. When the mediator binds to chemoreceptors, potassium or chloride chemodependent channels are activated. As a result, potassium ions exit the cell through the membrane. Chlorine ions enter through it. Only local hyperpolarization of the subsynaptic membrane occurs. It is called inhibitory postsynaptic potential (IPSP).
The value of EPSP and IPSP is determined by the number of mediator quanta released from the terminal, and hence the frequency of nerve impulses. Those. synaptic transmission is not subject to the all-or-nothing law. If the amount of excitatory mediator released is sufficiently large, then a propagating AP can be generated in the subsynaptic membrane. IPSP, regardless of the amount of mediator, does not extend beyond the subsynaptic membrane.
After the cessation of the flow of nerve impulses, the released neurotransmitter is removed from the synaptic cleft in three ways:
1. It is destroyed by special enzymes fixed on the surface of the subsynaptic membrane. In cholinergic synapses, it is acetylcholinesterase (AChE). In adrenergic, dopaminergic, serotonergic - monoamine oxidase (MAO) and catechol-o-methyltransferase (COMT).
2. Part of the neurotransmitter returns to the presynaptic ending using the reuptake process (the meaning is that the synthesis of a new neurotransmitter is a long process).
3. A small amount is carried away by the intercellular fluid.
Features of the transmission of excitation through chemical synapses:
1. Excitation is transmitted in only one direction, which contributes to its precise distribution in the central nervous system.
2. They have a synaptic delay. This is the time required for the release of the mediator, its diffusion and processes in the subsynaptic membrane.
3. Transformation occurs in synapses, i.e. change in the frequency of nerve impulses.
4. They are characterized by the phenomenon of summation. Those. the higher the pulse frequency, the higher the amplitude of the EPSP and IPSP.
5. Synapses have low lability.
Peripheral synapses are formed by the terminals of the efferent nerves and sections of the membranes of the executive organs. For example, neuromuscular synapses are formed by the axon endings of motor neurons and muscle fibers. Due to their peculiar shape, they are called neuromuscular end plates. Their general structural plan is the same as that of all chemical synapses, but the subsynaptic membrane is thicker and forms numerous subsynaptic folds. They increase the area of synaptic contact. The mediator of these synapses is acetylcholine. H-cholinergic receptors are built into the subsynaptic membrane, i.e. cholinergic receptors, which, in addition to ACh, can also bind to nicotine. The interaction of acetylcholine with cholinergic receptors leads to the opening of chemodependent sodium channels and the development of depolarization. Due to the fact that individual quanta of acetylcholine are also released at rest, weak short-term bursts of depolarization constantly occur in the postsynaptic membrane of neuromuscular synapses - miniature end plate potentials (MEPPs). Upon receipt of a nerve impulse, a large amount of ACh is released and a pronounced depolarization develops, called the end plate potential (EPP). In contrast to the central ones, in the neuromuscular synapses, the PKP is always significantly higher than the critical level of depolarization. Therefore, it is always accompanied by PD generation and muscle fiber contraction. Those. for spreading excitation and reducing the summation of the effects of neurotransmitter quanta is not required. Curare poison and curare-like drugs pharmacological drugs sharply reduce PKP and block neuromuscular transmission. As a result, all skeletal muscles, including respiratory ones, are turned off. This is used for mechanically ventilated surgeries. Destruction of ACh is carried out by the enzyme acetylcholinesterase. Some organophosphates (chlorophos, sarin) inactivate cholinesterase. Therefore, ACh accumulates in synapses and muscle cramps occur.
Concept definition
Local potential (LP) is a local non-spreading subthreshold excitation that exists in the range from the resting potential (-70 mV on average) to the critical level of depolarization (-50 mV on average). Its duration can be from several milliseconds to tens of minutes.
In case of exceeding critical level of depolarization local potential goes into action potential and generates .
Critical level of depolarization (KUD) - this is the level of the electrical potential of the membrane of an excitable cell, from which the local potential becomes an action potential. The transition of the local potential to the action potential is based on the self-increasing opening of voltage-gated ion channels for sodium, which occurs under the influence of increasing depolarization. Thus, CUD reveals, in addition to the previously discovered ion channels, another group of sodium ion channels - the potential of controlled ones.
The FCA is usually -50 mV, but it varies from neuron to neuron and can change as the excitability of the neuron changes. The closer the FRC is to the resting potential (-70 mV) and vice versa, the closer the resting potential is to the RCC, the more excitable the neuron is.
It is important to understand what the process of local potential generation begins with the opening of ion channels . Opening ion channels is the most important thing! They need to be opened in order for a stream of ions to enter the cell and bring electric charges into it. These ionic electric charges just cause the electric potential of the membrane to shift up or down, i.e. local potential.
sodium (Na+)
, then positive charges enter the cell along with sodium ions, and its potential shifts upward towards zero. It's depolarization and that's how it's born excitatory local potential
. It can be said that excitatory local potentials are generated by sodium ion channels when they open.
Figuratively, you can say this: "Channels open - potential is born."
If ion channels open for chlorine (Cl-) , then negative charges enter the cell together with chlorine ions, and its potential shifts down below the rest potential. This is hyperpolarization, and in this way braking local potential . It can be said that inhibitory local potentials generated by chloride ion channels.
There is also another mechanism for the formation of inhibitory local potentials - due to the opening of additional ion channels for potassium (K+) . In this case, "extra" portions of potassium ions begin to leave the cell through them, they carry positive charges and increase the electronegativity of the cell, i.e. cause hyperpolarization. Thus, it can be said that inhibitory local potentials are generated by additional potassium ion channels.
As you can see, everything is very simple, the main thing is to open the necessary ion channels . Stimulus-gated ion channels open with a stimulus (stimulus). Chemo-gated ion channels are opened by a neurotransmitter (excitatory or inhibitory). More precisely, depending on which channels (sodium, potassium or chloride) the mediator will act on, this will be the local potential - excitatory or inhibitory. And the mediator, both for excitatory local potentials and for inhibitory ones, can be the same, it is important here which ion channels will bind to it with their molecular receptors - sodium, potassium or chloride.
Types of LP:
1. Receptor. Occurs on receptor cells (sensory receptors) or receptor endings of neurons under the influence of a stimulus (stimulus). The mechanism of the emergence of such a receptor local potential is considered in detail on the example of sound perception by auditory receptors - Molecular mechanisms of sound reception (transduction) point by point This process is called "transduction", that is, the transformation of irritation into nervous excitation. Sensory receptors of the secondary type are not able to generate a nerve impulse, therefore their excitation remains local and how much the receptor cell will throw out the mediator depends on its amplitude.
2. Generator . Occurs on sensory afferent neurons (on their dendritic endings, nodes of Ranvier and / or axon hillocks) under the action of mediators that have isolated sensory cellular receptors of the secondary type. The generator potential turns into an action potential and a nerve impulse when it reaches a critical level of depolarization, i.e. He generates(generates) a nerve impulse. That is why it is called generator.
3. Excitatory postsynaptic potential (EPSP) . Occurs on the postsynaptic membrane of the synapse, i.e. it reflects the transfer of excitation from one neuron to another. Usually it is +4 mV. It is important to note that excitation is transmitted from one neuron to another precisely in the form of an EPSP, and not a ready-made nerve impulse. EPSP causes a depolarization of the membrane, but subthreshold, not reaching the KUD and not able to generate a nerve impulse. Therefore, a whole series of EPSPs is usually required in order for a nerve impulse to be born, because. the value of a single EPSP is completely insufficient to reach a critical level of depolarization. You can calculate for yourself how many simultaneous EPSPs are required to generate a nerve impulse. (Answer: 5-6.)
4. Inhibitory postsynaptic potential (IPSP) . Occurs on the postsynaptic membrane of the synapse, but only does not excite it, but, on the contrary, inhibits it. Accordingly, this postsynaptic membrane is part of inhibitory synapse and not exciting. IPSP causes membrane hyperpolarization, i.e. shifts the resting potential down, away from zero. Usually it is -0.2 mV. There are two mechanisms for creating TSSP: 1) "chloric" - there is an opening of ion channels for chlorine (Cl-), through them chloride ions enter the cell and increase its electronegativity, 2) "potassium" - there is an opening of ion channels for potassium (K +), potassium ions come out through them, carry away positive charges from the cell, which increases the electronegativity in the cell.
5. Pacemaker Potentials - these are endogenous close to sinusoidal periodic oscillations of the membrane potential with a frequency of 0.1-10 Hz and an amplitude of 5-10 mV. They are generated by special pacemaker neurons (pacemakers) on their own, without external influence. Pacemaker local potentials ensure that the neuron-pacemaker periodically reaches a critical level of depolarization and spontaneous (i.e., spontaneous) generation of action potentials and, accordingly, nerve impulses.
Where do local potentials (LP) occur?
The answer is simple: on sensory receptors, on the dendritic receptor endings of neurons, and on the postsynaptic membranes of synapses. We should not forget the axon hillock, where local potentials are integrated and create a generator potential that generates a nerve impulse. There they should be looked for in order to give examples of LP.
Places of occurrence of local potentials:
1. Sensory cell receptors (for example, auditory hair cells, taste buds, etc.).
2. Receptor endings of sensitive (afferent) neurons (for example, nociceptors of pain neurons).
3. Postsynaptic membranes of synaptic contacts.
4. The generator potential is formed on the axon hillock.
Characteristics of membrane potentials
Indicators | Receptor potential | Post-synaptic potential (EPSP or IPSP) | action potential |
| Localization (location) | Membrane of a sensory receptor cell or receptor ending of an afferent neuron. | The postsynaptic membrane of the synapse. | Occurrence: axon hillock, intercept of Ranvier, postsynaptic membrane of the synapse. Distribution: throughout the membrane of the neuron. |
| Origin mechanism | Opening of stimulus-gated ion channels for sodium. | Opening by a mediator of chemo-controlled ion channels for sodium (EPSP) or for chlorine or potassium (TPSP). | Opening of voltage-gated ion channels for sodium. |
Amplitude | |||
Duration | 5 ms - 20 min | ||
Amplitude: time/space | Decreasing. | Decreasing. | Continuous. |
Movement | Local. | Local. | Propagating. |
| Functional dependence: impact force / amplitude | The magnitude (amplitude) depends on the strength of the stimulus. | The value (amplitude) depends on the amount of neurotransmitter acting on the postsynaptic membrane. | The amplitude is standard for a given neuron and does not depend on the strength of the stimulus or on the amount of the neurotransmitter. |
Properties of local potentials
1. Local potential is directly proportional the strength of the stimulus which calls it.
2. Local potentials are limited during time(do not last long) size(do not grow large) and space(do not run anywhere).
3. Local potentials are capable of summation ., i.e. they combine and give an increased value (amplitude).
4. The amplitude of the local potential decreases in direct proportion to the square of the distance. This means that the LP does not cover the entire membrane of the neuron, but is limited to the area where it originated. Although, nevertheless, many individual LPs are summed up and collectively act on the axon colliculus, creating a generator potential.
