Long-term synaptic facilitation in defensive behavior command neurons in the snail during acquisition of sensitization depends on RNA synthesis.

Experiments on defensive behavior command neuron LP11 in semi-intact common snails preparations were performed to study transcription processes underlying the mechanisms of neuronal plasticity during acquisition of nociceptive sensitization. Application of nociceptive stimuli to the heads of control snails led to increases in neuron membrane excitability, along with biphasic changes in responses to tactile and chemical sensory stimulation--with depressed responses at the short-term stage and facilitation in the long-term stage of sensitization. Acquisition of sensitization after application of the RNA synthesis inhibitor actinomycin D (20 microM) to neuron LP11 led to complete suppression of synaptic facilitation in responses to sensory stimulation in the long-term stage of sensitization, but had no effect on the short-term depression of responses. However, the inhibitor had no effect on changes in membrane excitability in these conditions. Application of actinomycin D 30 min after the end of the sensitization acquisition process (1 h after the process started) had no effect on membrane excitability or synaptic facilitation. It is suggested that the induction of long-term synaptic facilitation in neuron LP11 during acquisition of nociceptive sensitization is dependent on RNA synthesis occurring in a narrow time interval, while changes in membrane excitability during the 2-3 h after acquisition of sensitization and short-term synaptic plasticity are independent of transcription processes.