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Experiments on semi-intact preparations from common snails were used to study the characteristics of the actions of MK-801, an antagonist of NMDA glutamate receptors, on the plasticity of various sensory inputs to defensive behavior command neurons LPl1 and RPl1 during acquisition of nociceptive sensitization. Application of sensitizing stimuli to the head or foot of control snails led to depression of neuron responses to tactile and chemical sensory stimulation during the short-term stage and marked facilitation of these responses during the long-term stage of sensitization. Application of sensitizing stimuli to the snail's head during administration of MK-801 led to marked depression of responses to chemical stimulation of the head in both the short-term and long-term stages of sensitization. In addition, blockade of NMDA receptors during application of sensitizing stimuli to the foot or head had no effect on changes in neuron responses elicited by chemical stimulation of the snail's foot and by tactile stimulation of the foot or head. It is suggested that NMDA-like glutamate receptors are selectively involved in the mechanism of induction of plasticity of synaptic inputs to command neurons LPl1 and RPl1, excited by chemical sensory stimulation of the head – a skin receptor zone specific for these neurons.