Long-term benzodiazepine treatment reduces neuronal responsiveness to cholecystokinin: an electrophysiological study in the rat.
Acute benzodiazepine administration has been reported to antagonize the effect of cholecystokinin both in the periphery and in the central nervous system. A two-week treatment with either diazepam (5 mg/kg per day) or flurazepam (15 mg/kg per day) markedly reduced the excitatory effect of microiontophoretically applied sulphated cholecystokinin octapeptide-(26-33) on rat CA3 hippocampal pyramidal neurons but not that of acetylcholine. In view of the sustained anxiolytic activity of benzodiazepines that contrasts with their transient sedative effect, the present results suggest that the reduction of neuronal responsiveness to cholecystokinin by these drugs might be related to their anxiolytic property.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology*; D002766:Cholecystokinin / Q000494:pharmacology*; D003975:Diazepam / Q000494:pharmacology; D004594:Electrophysiology; D005479:Flurazepam / Q000494:pharmacology; D006624:Hippocampus / Q000502:physiology; D007478:Iontophoresis; D008297:Male; D009474:Neurons / Q000187:drug effects*; D011712:Pyramidal Tracts / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D014151:Anti-Anxiety Agents; D002766:Cholecystokinin; D005479:Flurazepam; D000109:Acetylcholine; D003975:Diazepam