Selective involvement of opioids in the mechanisms of synapse-specific plasticity in the common snail during the acquisition of sensitization

Abstract

Studies on defensive behavior command neurons LP11 and RP11 in semi-intact common snail preparations were performed to investigate the effects of the opioid peptide met-enkephalin and the opioid antagonist naloxone on the effects of nociceptive sensitization. Application of nociceptive stimuli to the snail's head elicited marked reversible membrane depolarization along with depression of neuron responses to sensory stimulation during the short-term stage of sensitization and facilitation of responses in the long-term stage. Met-enkephalin at a dose of 10 microM but not at a dose of 0.1 microM partially suppressed responses to nociceptive stimuli. Acquisition of sensitization during exposure to met-enkephalin at doses of 10 and 0.1 microM led to complete suppression of the facilitation of responses to tactile stimulation of the head. Facilitation of responses to chemical stimulation of the head and tactile stimulation of the foot in these conditions was similar to that of neurons in control sensitized animals. Acquisition of sensitization during exposure to met-enkephalin and/or naloxone elicited selective suppression of facilitation of responses to chemical stimulation of the head but had no effect on facilitation of responses to tactile stimulation of the head and foot. Met-enkephalin and naloxone had no effect on the depression of neuron responses evoked by sensory stimulation in the short-term stage of sensitization. It is suggested that during the acquisition of sensitization in the common snail, opioids are involved in controlling the mechanism of nociception and in the mechanisms of selective induction of long-term plasticity of the synaptic inputs to command neurons activated by tactile and chemical stimulation of the animal's head.