Receptor-mediated dopaminergic function after ethanol withdrawal.
Striatal dopamine (DA) synthesis, measured in vivo as accumulation of DOPA after aromatic amino acid decarboxylase inhibition, is increased by neuroleptics and decreased by DA agonists as a result of their interactions with regulatory receptors. A sensitive high performance liquid chromatography (HPLC) technique has been developed, which allows the evaluation of both increases and decreases in DOPA levels in response to agonists and antagonists, and simultaneously permits measurement of DA levels as an indication of DA neuronal activity. C57BL mice, after chronic ethanol treatment and withdrawal, demonstrate significantly decreased responses, in terms of DOPA accumulation and DA release, to both haloperidol, a DA antagonist, and apomorphine, a DA agonist. These effects cannot be interpreted as resulting either from DA receptor subsensitivity or supersensitivity, but suggest instead that coupling between DA receptors and tyrosine hydroxylase is perturbed by ethanol treatment.
D000437:Alcoholism / Q000503:physiopathology*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001921:Brain / Q000378:metabolism; D004295:Dihydroxyphenylalanine / Q000378:metabolism; D004298:Dopamine / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011954:Receptors, Dopamine / Q000502:physiology*; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D011954:Receptors, Dopamine; D004295:Dihydroxyphenylalanine; D014446:Tyrosine 3-Monooxygenase; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine