Serotonin decreases population spike amplitude in hippocampal cells through a pertussis toxin substrate.
Activation of the serotonin1A receptor decreases CA1 population spike amplitude and inhibits forskolin-stimulated adenylate cyclase in rat hippocampus. Pretreatment of rats with pertussis toxin blocked both responses. Because the electrophysiological and biochemical responses to serotonin were correlated after pertussis toxin treatment, we conclude that both responses are mediated by a common regulatory protein, presumably Gi.
D000200:Action Potentials / Q000187:drug effects; D037361:Adenylate Cyclase Toxin; D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D005576:Colforsin / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D037342:Pertussis Toxin; D051381:Rats; D011919:Rats, Inbred Strains; D011985:Receptors, Serotonin / Q000187:drug effects*; D012701:Serotonin / Q000502:physiology*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*
D037361:Adenylate Cyclase Toxin; D011985:Receptors, Serotonin; D010566:Virulence Factors, Bordetella; D005576:Colforsin; D012701:Serotonin; D037342:Pertussis Toxin; D000262:Adenylyl Cyclases