Abstract
Defensive behavior command neurons LP11 and RP11 were studied in semi-intact snail preparations to investigate the effects of N-methyl-D-aspartate (NMDA) receptor antagonists on the mechanisms of nociceptive sensitization. Application of sensitizing stimuli to the heads of control snails led to membrane depolarization and increased excitability, and also depressed the responses of neurons to tactile and chemical sensory stimuli in the short-term stage and facilitated responses in the long-term stage of sensitization. Development of sensitization in conditions of exposure to the NMDA receptor antagonists AP5 or MK-801 produced changes in the membrane potential and membrane excitability of command neurons similar to those seen in neurons of control sensitized snails. In addition, changes in the responses of command neurons to tactile stimulation of the head and foot and chemical stimulation of the foot in these conditions were also similar to those seen in neurons of control animals. Acquisition of sensitization during administration of NMDA receptor antagonists led to pronounced depression of responses to chemical test sensory stimulation of the snails' heads in both the short-term and long-term stages of sensitization. Thus. in sensitized snails. NMDA glutamate receptor antagonists selectively acted on the mechanisms of induction of plasticity the synaptic "inputs" of command neurons mediating excitation from chemical sensory stimuli from the animal's head.