inhibition(redirected from endproduct inhibition)
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in biology, an active nervous process that leads to the suppression or prevention of excitation. A distinction is made between peripheral inhibition, which takes place in the synapses and directly affects the muscular and glandular elements, and central inhibition, which takes place within the central nervous system.
The best-known types of inhibition are based on the interaction between a mediator, secreted and discharged from presynaptic elements (usually nerve endings), and specific molecules of the postsynaptic membrane. Such interaction is accompanied by the postsynaptic membrane’s momentarily higher permeability to K+ and Cl– ions; this causes a reduction in the membrane’s electrical input impedance and in many cases also generates a hyper-polarizing inhibitory postsynaptic potential. As a result, the membrane’s excitability is diminished—an effect which may last from a few milliseconds in some cases to tens of milliseconds in others; thus the membrane is much less likely to be affected by the spreading excitation.
Inhibition always develops as a consequence of excitation of the corresponding inhibitory neurons. The postsynaptic effect may be excitatory or inhibitory, depending on changes in the postsynaptic membrane’s ionic permeability associated with the interaction between the mediators and the receptors. Some mediators can therefore be the means of both excitation and inhibition. For example, acetylcholine inhibits the fibers of the myocardium and excites the skeletal muscles in vertebrates. In the nerve ganglia of mollusks, the synapses of cholinergic neurons produce excitation in some cells and inhibition in others. In the view of several researchers, some mediators are specifically inhibitory—for example, glycine in the spinal cord and medulla oblongata or gamma-aminobutyric acid in the brain centers and peripheral synapses of crustaceans. Neurons with specific inhibitory functions have been discovered, such as the Renshaw cells in the spinal cord, Purkinje’s cells in the cerebellum, and the basket cells in the hippocampus, which is part of the limbic system. The synapses formed by these neurons have ultrastructural properties that make it possible to distinguish them from excitatory synapses. In some types of neurons, the dendrites and the areas adjacent to them are the locus of the inhibitory synapses; in this case, inhibition is found to be highly effective by virtue of proximity to the triggering zone in which excitation is initiated. There are exceptions to this rule—for example, the inhibitory synapses of stellate neurons on Purkinje’s cells in the cerebellum are located on remote sections of the dendrites.
The functional significance of postsynaptic inhibition is varied. Afferent (direct) inhibition serves to weaken the excitation of functionally antagonistic elements, thereby promoting a coordinated, spatially directed flow of excitation in chains of neurons. In the spinal cord in particular, this type of inhibition is the basis of reciprocal inhibition of the motoneurons that innervate antagonistic muscles. Collateral inhibition, which is effected through the reciprocal collaterals, or branches, of the axons of efferent neurons and specialized intercalary inhibitory neurons, stabilizes the proper level of excitation of a given structural-functional bloc of neurons and limits the spread of excitation to neighboring populations of neurons.
Fewer studies have been made of presynaptic inhibition—a term applied to the suppression of excitation in the nerve endings, or at the point of entry of the postsynaptic cellular element. This type of inhibition is of especially long duration, lasting some hundreds of milliseconds, and it coincides with the period of depolarization of incoming afferents. It is generally assumed that the basis of presynaptic inhibition is depolarization, and that the morphological substrate of presynaptic inhibition consists of axon-to-axon synapses, the origin of whose presynaptic elements is unknown. Convincing arguments have been presented for regarding gamma-aminobutyric acid as a mediator of presynaptic inhibition, at least in the neuromuscular synapses of crustaceans and in the spinal cord of vertebrates. Sechenov’s inhibition, as demonstrated in the frog, is apparently a function of presynaptic inhibition. Another type of inhibition is the secondary type, also known as pessimum; in the theory of parabiosis, this term is applied to the blocking of excessive excitation, as first described by N. E. Vvedenskii. It is difficult to elicit such inhibition under experimental physiological conditions, but the phenomenon can be demonstrated in abnormal (specifically, convulsive) states.
In his work on the conditioned reflex, I. P. Pavlov identified two types of inhibition: external inhibition is the inhibition of any ongoing activity by an orienting reflex in response to an extraneous stimulus, while internal inhibition refers to the extinction of conditioned reflexes, the differentiation of conditioned reflexes, or the formation of delayed and trace-conditioned reflexes. Another type of inhibition identified by Pavlov is protective inhibition, which prevents the overstimulation or overexhaustion of the nerve centers. Disruption of the relationship between inhibition and excitation results in various nervous and mental disorders.
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A. S. BATUEV and D. N. LENKOV