We present published data along with our own results concerning the role of second messengers and their intracellular receptors in molecular mechanisms associated with the plasticity of neurons during learning. The participation of cyclic 3',5'-adenosine monophosphate, cyclic 3',5'-guanosine monophosphate, calcium, calmodulin, and also the metabolic products of inositol phospholipids, inositol-1,4,5-triphosphate, diacylglycerol and the protein kinase C activated by it, arachidonic acid, and the products of its lipoxygenase oxidation during the regulation of neuronal plasticity over the course of prolonged potentiation, sensitization, habituation, and classical associative training are discussed.

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The possible role of cGMP in the regulation of the extinction of the reactions of the RPa4, RPa3, and LPa3 neurons of the edible snail in response to acetylcholine (ACh), applied rhythmically to the soma of the neuron by means of microiontophoresis, has been investigated. It was demonstrated that activators of guanylate cyclase which increased the level of cGMP in the cell, namely, sodium nitroprusside and sodium azide (5.10(-4)-10(-3) mole/liter), when applied intracellularly, intensify the extinction of inward transmembrane current and of depolarization of the membrane in response to ACh. The hypothesis of the participation of cGMP-dependent phosphorylation of membrane proteins in the regulation of the rate of development, depth, and duration of short-lived plasticity of the cholinoreceptors of the neuron is proposed.