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Ethanol Does Not Modify Opiate‐Mediated Inhibition of Striatal Adenylate Cyclase
Author(s) -
Hoffman Paula L.,
Tabakoff Boris
Publication year - 1986
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.1471-4159.1986.tb13044.x
Subject(s) - cyclase , adenylate kinase , opiate , chemistry , medicine , in vivo , endocrinology , receptor , biochemistry , biology , microbiology and biotechnology
Ethanol increases the activity of “basal,” guanine nucleotide‐and dopamine‐stimulated adenylate cyclase in mouse striatum. In contrast, ethanol, in vitro, did not modify the inhibition of striatal adenylate cyclase activity by opiates (morphine or [D‐Ala 2 , D‐Leu 5 ] enkephalin). Following chronic in vivo ethanol treatment of mice, there was also no change in the character of opiate inhibition of striatal adenylate cyclase activity. Since ethanol, in vitro, does decrease striatal opiate receptor binding, the results suggest that the changes in affinity detected by ligand binding studies are not relevant for receptor‐coupled adenylate cyclase activity, or that opiate receptor binding and opiate regulation of adenylate cyclase can be modulated independently. The selective effects of ethanol on systems that modulate adenylate cyclase activity may produce imbalances in neuronal function during in vivo ethanol exposure.