Choline and physostigmine enhance haloperidol-induced HVA and DOPAC accumulation.
Nigrostriatal neurons respond to dopamine receptor blockade by increasing their firing frequency. We observe that the concurrent administration to rats of cholinergic agonists and haloperidol, a dopamine receptor antagonist, produces a synergistic acceleration in striatal dopamine turnover. Doses of choline and physostigmine which, when given alone, have no effect, enhance the haloperidol-induced accumulation of the dopamine metabolites homovanillic acid and 3,4-dihydroxyphenylacetic acid. These results support the hypothesis that the extent to which nigrostriatal neurons are modulated by cholinergic receptor activation depends on their firing frequency.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism*; D000818:Animals; D002794:Choline / Q000494:pharmacology*; D003342:Corpus Striatum / Q000378:metabolism; D004357:Drug Synergism; D006220:Haloperidol / Q000494:pharmacology*; D006719:Homovanillic Acid / Q000378:metabolism*; D008297:Male; D010648:Phenylacetates / Q000378:metabolism*; D010830:Physostigmine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D010648:Phenylacetates; D015102:3,4-Dihydroxyphenylacetic Acid; D010830:Physostigmine; D006220:Haloperidol; D002794:Choline; D006719:Homovanillic Acid