Depletion of serotonin in the nervous system of Aplysia reduces the behavioral enhancement of gill withdrawal as well as the heterosynaptic facilitation produced by tail shock.

摘要: 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 dishabituation (if reflex been habituated) or sensitization it not habituated), might be mediated, at least in part, by endogenous monoaminergic transmitter serotonin (5-HT). To assess 5-HT's role of Aplysia withdrawal reflex, we treated with serotonergic neurotoxin 5,7- dihydroxytryptamine (5,7-DHT). We found 5,7-DHT treatment significantly reduced produced tail shock. Treatment also blocked heterosynaptic facilitation monosynaptic connections between siphon sensory neurons their follower cells, which contributes enhancement. Analysis high-performance liquid chromatography 5- HT levels CNS. Moreover, neurotoxic effects DHT appeared relatively specific for pathways. Thus, did disrupt ability nonserotonergic facilitatory interneurons, L29 facilitate neurons. Also, 5-HT-dependent, but dopamine-dependent, histofluorescence central ganglia. Finally, does reduce peptides SCPA SCPB within Our results, together those Mackey et al. (1989), indicate 5-HT plays a major mediating