Essence and role in the body
For a long time, it was believed that the cessation of activity was simply the absence of stimulating signals. However, it has been proven that inhibition is precisely an active biological process.
In the central nervous system (CNS) and internal organs, this process is inextricably linked with excitation. They are in a state of constant alternation, like a pendulum, which allows for precise regulation of the level of tissue activity.
Inhibition can occur in two ways:
- As an absolute independent functional process (purposeful suppression of activity).
- As a result of the interaction of two excitations (when one excitatory signal overlaps or extinguishes another).
History of study
The foundation of the doctrine of inhibitory processes was laid by classical physiological experiments of the 19th century. Historically and anatomically, two key lines of discovery are distinguished:
- Peripheral inhibition. Discovered by brothers A. and E. Weber in 1847. In their experiments, they demonstrated how stimulation of the vagus nerves leads to the slowing and cessation of heart function, proving that a nerve impulse can not only trigger but also inhibit organ function.
- Central inhibition. Occurs directly within the CNS structures. Its phenomenon was first thoroughly investigated and described by the prominent Russian physiologist I.M. Sechenov in 1862, turning the understanding of brain and spinal cord function upside down.
Classification by electrophysiological nature
At the cellular membrane level, inhibition is implemented through changes in electrical potentials. Depending on the mechanism, three main types of inhibition are distinguished.
1. Hyperpolarization inhibition
The most classic variant, developing on postsynaptic membranes.
- Mechanism: Caused by the direct action of specific inhibitory neurotransmitters.
- Result: Hyperpolarization develops (an increase in the negative charge inside the cell), which leads to a sharp decrease in tissue excitability. It becomes much harder for the cell to reach the activation threshold.
2. Persistent depolarization inhibition
Occurs as a paradoxical response to excessive stimulation.
- Cause: A very high frequency of incoming excitatory signals.
- Mechanism: Excessive accumulation of the excitatory neurotransmitter occurs in the synaptic cleft. This prevents the normal return of the membrane potential to its initial resting state.
- Physiological significance: The difference between the current membrane charge and the critical level of depolarization (CLD) increases significantly. The tissue "freezes" in an inactive state. Essentially, this process is closely similar to the phenomena of parabiosis or accommodation.
- Note: In some cases, this type of inhibition can also be triggered by inhibitory neurotransmitters, depending on the specific properties of a particular cell membrane.
3. Stabilization inhibition
Also known as stabilization of the resting potential.
- Cause: The action of certain biologically active substances.
- Mechanism: A rigid blockade of sodium permeability of the membranes occurs. Meanwhile, the resting potential itself remains unchanged.
- Result: Due to the impossibility of sodium ion current into the cell, the generation of a new action potential (excitation) becomes absolutely impossible.
Briefly: answers to topical questions
What is the ionic mechanism of hyperpolarization inhibition?
The ionic mechanism of hyperpolarization inhibition consists in a specific increase in the permeability of the postsynaptic membrane to potassium and chloride ions.
- Potassium — $K^+$ ions flow out of the cell.
- Chloride — $Cl^-$ ions enter the cell along the concentration gradient.
As a result of the directed movement of these ions, hyperpolarization of the postsynaptic membrane occurs and an inhibitory postsynaptic potential (IPSP) is formed. This leads to an increase in the excitation threshold, a drop in tissue excitability, and the blocking of excitation conduction.
Which specific neurotransmitters cause hyperpolarization inhibition?
Hyperpolarization inhibition is caused by certain inhibitory neurotransmitters, the localization of whose action depends on the division of the nervous system:
- GABA (gamma-aminobutyric acid) — acts in CNS synapses.
- Glycine — acts in CNS synapses.
- Acetylcholine — functions in inhibitory synapses of the autonomic nervous system.
- Norepinephrine — functions in inhibitory synapses of the autonomic nervous system.
How is central inhibition classified by its localization in the neuron?
According to its localization in the neuron, two main types of inhibition are distinguished:
- Presynaptic inhibition — localized in the axo-axonic synapse. The inhibitory neuron acts on the presynaptic terminal of the main axon, blocking the conduction of the impulse before it reaches the synapse with the main cell.
- Postsynaptic inhibition — usually localized in the axo-somatic synapse. The inhibitory neuron directly acts on the cell body (soma), causing direct inhibition of the postsynaptic neuron.
What is pessimistic inhibition according to Vvedensky?
Pessimistic (secondary) inhibition according to N.E. Vvedensky is a phenomenon where, due to the stimulus frequency exceeding the measure of tissue lability, instead of the expected increase in contraction amplitude, its decrease is noted. It develops at a high frequency of stimulation, when each subsequent impulse falls into the repolarization (relative refractory) phase of the previous cycle. The mechanism may be based on an excess of neurotransmitter causing sustained membrane depolarization. This type of inhibition performs an important protective and restorative function.
Remembering the three types of membrane inhibition is helped by the rule "GDS": Hyperpolarization (charge goes negative), Depolarization (neurotransmitter accumulated, membrane "froze"), Stabilization (sodium blocked, resting potential frozen).
Class and exam questions
Is inhibition a passive process of signal extinction?
No. It is an exclusively active biological process that requires energy expenditure and purposefully terminates or prevents excitation from developing.
Why does a cell stop firing during persistent depolarizing inhibition if depolarization is a sign of excitation?
Due to the excessively high frequency of impulses, the neurotransmitter accumulates, and the membrane does not have time to return to the resting state. At the same time, the critical level of depolarization (CLD) moves away from the current membrane charge, making a new impulse impossible.
What is the main difference between stabilizing inhibition and hyperpolarizing inhibition?
In stabilization inhibition, the resting membrane potential remains unchanged, and sodium permeability is simply blocked. In hyperpolarization inhibition, the membrane charge is artificially lowered by inhibitory neurotransmitters.
What else to study on this topic
- Mechanisms of action of inhibitory neurotransmitters on the postsynaptic membrane
- Interaction of two excitations as a cause of inhibition development
- Phenomena of parabiosis and accommodation in tissues
- Weber brothers' experiment: the effect of the vagus nerve on heart activity
- Sechenov's experiment and the phenomenon of central inhibition
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