Noxious stimuli, such as electrical shocks to the animal's tail, enhance Aplysia's gill-and siphon-withdrawal reflex. Previous experimental work has indicated that this behavioral enhancement, known as dishabituation (if the reflex has been habituated) or sensitization (if it has not been habituated), might be mediated, at least in part, by the endogenous monoaminergic transmitter serotonin (5HT). To assess 5-HT's role in dishabituation and sensitization of Ap/ysia withdrawal reflex, we treated

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... Apiysia with the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). We found that 5,74HT treatment significantly reduced the dishabituation of the withdrawal reflex produced by tail shock. Treatment with the neurotoxin also blocked the heterosynaptic facilitation of monosynaptic connections between siphon sensory neurons and their follower cells, which contributes to the behavioral enhancement. Analysis by high-performance liquid chromatography indicated that 5,7-DHT treatment significantly reduced 5-HT levels in the Ap/ysia CNS. Moreover, the neurotoxic effects of 5,7-DHT appeared to be relatively specific for serotonergic pathways. Thus, 5,7-DHT treatment did not disrupt the ability of nonserotonergic facilitatory intemeurons, the L29 cells, to facilitate the connections of siphon sensory neurons. Also, 5,7-DHT reduced 5-HT-dependent, but not dopamine-dependent, histofluorescence in Apiysia central ganglia. Finally, 5,7-DHT does not reduce the levels of the facilitatory peptides SCP, and SCP, within the Aplysia CNS. Our results, together with those of Mackey et al. (1989) , indicate that 5-HT plays a major role in mediating dishabituation and sensitization of Aplysia's withdrawal reflex. A variety of experimental evidence suggests that the monoamine serotonin (5HT) mediates short-term behavioral dishabituation and sensitization of Aplysia's gill-and siphon-withdrawal response. Application of 5-HT mimics the known facilitatory effects of dishabituating or sensitizing stimuli (such as electrical