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Modulation of In Vivo Dopamine Release by D 2 but Not D 1 Receptor Agonists and Antagonists
Author(s) -
Boyar William C.,
Altar C. Anthony
Publication year - 1987
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.1471-4159.1987.tb05591.x
Subject(s) - dopamine , in vivo , chemistry , modulation (music) , dopamine receptor , pharmacology , receptor , neuroscience , biology , biochemistry , physics , acoustics , microbiology and biotechnology
The capacity of D 1 and D 2 agonists and antagonists to regulate the in vivo release and metabolism of dopamine (DA) in mesolimbic and nigrostriatal DA neurons of the mouse was determined using gas chromatographic and mass fragmentographic (GC‐MF) analysis. DA release was inferred from levels of 3‐methoxytyramine (3‐MT) and DA metabolism was inferred from levels of 3,4‐dihydroxyphen‐ylacetic acid (DOPAC) and homovanillic acid (HVA). DA release was increased by the D 2 antagonists haloperidol and metoclopramide but not by the D 1 antagonists SCH 23390 and SKF 83566. DA metabolism was increased by each of the four antagonists but to a greater extent with the D 2 antagonists. The D 2 agonists CGS 15855A and LY 171555 decreased DA release whereas the D 1 agonist SKF 38393, at relatively high doses, only slightly affected DA release. Each of the three agonists decreased DA metabolism but again metabolism was more affected by the D 2 ‐selective drugs. The in vivo release of DA from mesolimbic and neostriatal DA neurons appears to be modulated by D 2 but not by D 1 receptors, whereas both receptor types can modulate DA metabolism.