Stimuli that produce sensitization lead to elevation of cyclic AMP levels in tail sensory neurons of Aplysia.
Facilitation of synaptic connections between sensory neurons and motor neurons mediating the tail withdrawal reflex in Aplysia is produced by the modulatory effects of sensitizing stimuli. Facilitation can be mimicked by perfusing these neurons with serotonin (5-HT) in a semi-intact preparation. Consequently, 5-HT has been presumed to be acting as an agonist of the modulatory transmitter that mediates sensitizing input in vivo. While the 5-HT effects appear to be mediated by increased cyclic adenosine monophosphate (cAMP) levels in the sensory neurons, a critical issue that has not been examined is whether sensitizing stimuli also increase cAMP levels in these cells. We now report that such sensitizing stimuli delivered to the tail of a semi-intact preparation lead to elevation of cAMP levels in the tail sensory neurons.
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D000818:Animals; D001048:Aplysia; D000242:Cyclic AMP / Q000032:analysis*; D005724:Ganglia / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D009475:Neurons, Afferent / Q000032:analysis; D009479:Neuropeptides; D018377:Neurotransmitter Agents / Q000502:physiology; D009842:Oligopeptides / Q000494:pharmacology; D012018:Reflex / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology; D009435:Synaptic Transmission
D009479:Neuropeptides; D018377:Neurotransmitter Agents; D009842:Oligopeptides; D012701:Serotonin; C041307:small cardioactive peptide B; D000242:Cyclic AMP