A single identified interneuron gates tail-shock induced inhibition in the siphon withdrawal reflex of Aplysia.

The marine mollusc Aplysia has proven very useful for a mechanistic analysis of behavioral modification. Among the stimuli used to modify the behavior of Aplysia, a noxious stimulus, tail shock, is one of the most effective. In addition to the extensively analyzed facilitatory effects of tail shock, recent work has demonstrated that it also produces marked transient inhibition in reflex responses. Here we report that functional removal (by hyperpolarization or voltage clamp) of a single inhibitory interneuron, L16, can eliminate most, if not all, of the inhibition in the siphon withdrawal reflex circuit produced by tail shock. In addition, this interneuron is strongly activated by tail shock. Finally, direct intracellular activation of L16 does not, in itself, reliably produce inhibition, suggesting that L16 plays a gating role which is necessary for the expression of inhibition in the siphon withdrawal circuit. These results support the idea that behaviorally relevant neural modulation can be gated by a small number of neurons, in this case, by a single identified cell. Moreover, they indicate that in Aplysia, as in many other systems, the modulatory effects of a noxious stimulus are often funneled through a restricted neural locus before being distributed to the circuits actually responsible for generating the behavioral output.