Published data indicate that the synaptic inputs to defensive behavior command neurons in the common snail are cholinergic [6, 10] and glutamatergic [12]. The presence of pharmacologically similar postsynaptic and extrasynaptic cholinoreceptors in command neuron membranes [6,8,10] provides an approach to studying the postsynaptic mechanism of plasticity in command neurons in conditions of artificial activation of extrasynaptic cholinoreceptors, such that uncontrollable changes in transmitter release from the presynapse in conditions of electrical stimulation of the synaptic inputs can be excluded. Local application of constant-size portions of acetylcholine (ACh) to the body surface from an injection micropipette, operating as an artificial presynapse substituting for a presynaptic terminal, results in stable stimulation of a zone of the membrane containing extrasynaptic cholinoreceptors. The stimulation protocol for extrasynaptic cholinoreceptors imitates the stimulation scheme inducing habituation of the animal's defensive reactions [5]. Rhythmic application of ACh in these conditions leads to reversible depression of the evoked influx current (the ACh current), which reflects a decrease in the ACh sensitivity of the membrane [5].We have previously demonstrated that depression of the cholinosensitivity of the extrasynaptic zones of defensive behavior command neuron membranes in the common snail in a cellular analog of habituation results from a decrease in the number of membrane cholinoreceptors in the test zone [4]. Transport processes (endocytosis and exocytosis, underlying the internalization and recycling of receptors respectively) mediate these changes on the somatic membranes of neurons, with involvement of cytoskeletal elements, i.e., The involvement of cytoskeletal motor proteins, i.e., myosins, in the molecular mechanism of depression of the acetylcholine sensitivity of defensive behavior command neurons was studied in the common snail. Thus, the effects of compounds impairing myosin functioning on ACh-evoked current depression curves in neurons were studied -the myosin light chain kinase blockers ML-7 and MLCK-IP-18, the non-muscle myosin II inhibitor blebbistatin, and the ROCK-I and ROCK-II kinase (which mainly activate non-muscle myosin II) inhibitor Y-27632. ML-7 and MLCK-IP-18 were found to weaken depression of the current, while blebbistatin and Y-27632 had no effect on depression. The experimental results and mathematical models of the effects of these blockers on the number of membrane-bound cholinoreceptors suggest the involvement of myosins (except non-muscle myosin II) in the endo-and exocytosis of cholinoreceptors and the resultant depression of the cholinosensitivity of the somatic membranes of neurons in a cellular analog of habituation.