Dopaminergic regulation of cortical acetylcholine release.
The extent to which the activity of basal forebrain cholinergic neurons is influenced by dopamine (DA) was investigated using in vivo microdialysis of cortical acetylcholine (ACh). Systemic administration of the DA receptor agonist apomorphine significantly increased dialysate concentrations of ACh. Systemic, but not local, administration of d-amphetamine produced similar effects. Both D1 (SCH 23390) and D2 (haloperidol, raclopride) DA receptor antagonists attenuated the amphetamine-induced increase in cortical ACh release; however, only the D1 antagonist significantly reduced basal output of cortical ACh. These findings suggest that the activity of cortically projecting cholinergic neurons in the nucleus basalis is regulated in an excitatory manner by central dopaminergic neurons and that both D1 and D2 receptors are involved.
Day
J
J
Department of Psychiatry, University of British Columbia, Vancouver, Canada.
Fibiger
H C
HC
D000109:Acetylcholine / Q000378:metabolism*; D000661:Amphetamine / Q000494:pharmacology; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D002540:Cerebral Cortex / Q000378:metabolism*; D003956:Dialysis / Q000379:methods; D004298:Dopamine / Q000502:physiology*; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D006220:Haloperidol / Q000494:pharmacology; D008297:Male; D020891:Raclopride; D051381:Rats; D017208:Rats, Wistar; D012457:Salicylamides / Q000494:pharmacology
D001552:Benzazepines; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D012457:Salicylamides; D020891:Raclopride; D000661:Amphetamine; D006220:Haloperidol; D000109:Acetylcholine; D004298:Dopamine