The transient stage of long-term synaptic facilitation in defensive behavior command neurons in sensitized snails.

Experiments on common snails showed that three exposures to sensitizing stimuli (10% quinine applied to the snail's head every 15 min) induced synaptic facilitation in defensive behavior command neurons LPI1 and RPI1, with facilitation of responses to sensory stimuli lasting more than 24 h. Application of single stimuli produced transient synaptic facilitation and was expressed in responses to tactile stimulation of the head for about 1 h and in responses to dilute quinine for 3 h. Serotonin and cAMP imitated stimulus-specific transient synaptic facilitation. These substances facilitated the responses of neurons LPI1 and RPI1 to test stimulation of the head without producing changes in the responses to stimulation of other areas of skin on the animal's body. Calmodulin antagonists and glutamate NMDA receptor antagonists inhibited sensitization-induced synaptic facilitation in command neurons. Expression of transient synaptic facilitation depended on protein synthesis-it was suppressed by anisomycin and cycloheximide. It is suggested that transient synaptic facilitation during the acquisition of sensitization is associated with activation of translation/transcription processes and subsequent synthesis of specific short-lived protein molecules with selectively regulate the synaptic "inputs" of command neurons LPI1 and RPI1 from their specific skin innervation zones on the snail's head.