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Dopaminergic regulation of cortical acetylcholine release
Author(s) -
Day Jamie,
Fibiger Hans C.
Publication year - 1992
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890120405
Subject(s) - acetylcholine , sch 23390 , nucleus basalis , raclopride , apomorphine , dopaminergic , chemistry , cholinergic neuron , basal forebrain , cholinergic , microdialysis , dopamine , agonist , medicine , endocrinology , neuroscience , receptor , biology
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 D 1 (SCH 23390) and D 2 (haloperidol, raclopride) DA receptor antagonists attenuated the amphetamine‐induced increase in cortical ACh release; however, only the D 1 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 D 1 and D 2 receptors are involved. © 1992 Wiley‐Liss, Inc.