Neuronal mechanisms of reconsolidation of an associative aversive skill to food in the common snail.

We have previously established that reactivation of a long-term memory "trace" during exposure to a protein synthesis inhibitor in common snails trained to refuse a defined foodstuff impairs reproduction of this skill. In the present studies, the cellular mechanisms of memory reactivation were studied in defensive behavior command neurons LPl1 and RPl1 in snails. In the first series of experiments, the mechanisms of induction of amnesia were studied in semi-intact preparations 24 h after training of snails to refuse one foodstuff. These experiments showed that depression of the synaptic response to the conditioned stimulus developed 2.5 h after reminding (presentation of the conditioned food stimulus) on the background of exposure to cycloheximide. The second series of experiments addressed the neuronal mechanisms of development of amnesia. Animals were trained to refuse two foodstuffs. The snails were injected with cycloheximide 24 h after training and were subjected to the reminding procedure using one of the conditioned food stimuli. Semi-intact preparations were made 1, 3, 7, and 15 days after cycloheximide and the reminder. Responses to the conditioned food stimulus used as the reminder gradually decreased on days 1, 3, and 7. On days 7 and 15, measures of the responses to this conditioned stimulus were no different from those to the differential signal and were significantly smaller than responses to the second conditioned stimulus, which was not used as reminder. It is suggested that one of the cellular mechanisms of amnesia following impairment of long-term memory reconsolidation in snails consists of a specific, protein synthesis-dependent change in the efficiency of the synaptic connections of command neurons LPl1 and RPl1.