Forskolin mimics and blocks a serotonin-sensitive decreased K+ conductance 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 sensitizing stimuli. These effects can be mimicked by perfusing the pleural and pedal ganglia of a semi-intact preparation with serotonin (5-HT). In addition to the synaptic facilitation, 5-HT produces a depolarization associated with an increase in input resistance in the sensory neurons. The 5-HT-induced changes appear to be mediated by an elevation in cAMP levels. To examine further the role of cAMP in mediating the 5-HT response we utilized the potent cyclase activator forskolin. Forskolin mimics the 5-HT response and blocks the response to subsequent 5-HT applications indicating that both 5-HT and forskolin act through a common saturable mechanism. Voltage clamp and ion substitution experiments indicate that the 5-HT response is due, at least in part, to a decrease in a resting K+ conductance.
D000818:Animals; D001048:Aplysia; D005576:Colforsin; D000242:Cyclic AMP / Q000502:physiology*; D004224:Diterpenes / Q000494:pharmacology*; D005724:Ganglia / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology; D011188:Potassium / Q000502:physiology*; D012701:Serotonin / Q000502:physiology*; D009435:Synaptic Transmission
D004224:Diterpenes; D007473:Ion Channels; D005576:Colforsin; D012701:Serotonin; D000242:Cyclic AMP; D011188:Potassium