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In Vivo Striatal Dopamine Release by M1 Muscarinic Receptors Is Induced by Activation of Protein Kinase C
Author(s) -
Xu Mann,
Yamamoto Toshifumi,
Kato Takeshi
Publication year - 1990
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.1471-4159.1990.tb04891.x
Subject(s) - muscarinic acetylcholine receptor , chemistry , dopamine , in vivo , dopamine receptor , muscarinic acetylcholine receptor m4 , dopamine receptor d1 , pharmacology , protein kinase c , receptor , microbiology and biotechnology , neuroscience , phosphorylation , biology , biochemistry
Islet‐activating protein was unilaterally microinjected into rat stratum, and a dialysis cannula was implanted into the same area under anesthesia. After 2 days, various agents were perfused continuously into the striatum through the dialysis membrane, under freely moving conditions. Isletactivating protein (2 μg/2 μ1) treatment alone did not change in vivo striatal dopamine (DA) release and metabolism, but completely abolished the increase of striatal DA release evoked in vivo by the M1‐selective agonist McN‐A‐343 (10 −7 M ). Forskolin (10 −5 M ), an adenylate cyclase activator, increased DA release and showed an additive effect on the DA release evoked by McN‐A‐343. Polymyxin B, a rather selective inhibitor of protein kinase C, decreased DA release and completely blocked the effect of McN‐A‐343. These results suggest that in vivo striatal DA release elicited by M1 muscarinic receptors is coupled with interaction with a G protein and is induced by activation of protein kinase C.