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Dopamine Depletion Preferentially Impairs D 1 over D 2 ‐Receptor Regulation of Striatal In Vivo Acetylcholine Release
Author(s) -
Bertorelli Rosalia,
Zambelli Matilde,
Chiara Gaetano Di,
Consolo Silvana
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb08911.x
Subject(s) - acetylcholine , sch 23390 , dopamine , dopaminergic , endocrinology , chemistry , medicine , neurotransmitter , antagonist , neurotransmission , in vivo , inhibitory postsynaptic potential , receptor , biology , biochemistry , microbiology and biotechnology
The roles of D 2 and D 1 dopaminergic receptors on the regulation of striatal acetylcholine (ACh) release in vivo were examined for a period of 120 min after acute (2 h) or prolonged (16 h) depletion of brain dopamine (DA) by a‐ methyl‐ p ‐tyrosine. The reduction of DA transmission did not affect basal ACh output after 2 h but markedly lowered ACh release by 16 h (50%). Acute α‐methyl‐ p ‐tyrosine pre‐treatment prevented the reduction of ACh release by the D, antagonist SCH 23390 and its increase by the D 2 antagonist, remoxipride, consistent with a drastic reduction of DA transmission at both DA receptors. However, 16 h after α‐methyl‐ p ‐tyrosine, the effect of remoxipride on ACh release was restored, but SCH 23390 still had no effect, suggesting that the D 2 inhibitory tone on ACh release had recovered, whereas the reduction of the D 1 facilitatory influence persisted. The D 1 facilitatory control of ACh neurotransmis‐sion thus appears to be more sensitive than the D 2 inhibitory control to a reduction in DA transmission. The new model of DA‐ACh interaction resulting from these data casts fresh light on the relationship between changes in DA transmission and extrapyramidal motor function.