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Long‐Term Effects of Chronic Ethanol on Muscarinic Receptor Binding in Rat Brain
Author(s) -
Rothberg Brad S.,
Hunter Bruce E.,
Walker Don W.,
Anderson Jonathon F.,
Anderson Kevin J.
Publication year - 1996
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1996.tb01706.x
Subject(s) - quinuclidinyl benzilate , muscarinic acetylcholine receptor , neocortex , endocrinology , medicine , striatum , chemistry , hippocampus , agonist , antagonist , muscarinic antagonist , carbachol , cholinergic , ethanol , dentate gyrus , muscarinic acetylcholine receptor m4 , receptor , neuroscience , biology , biochemistry , dopamine
Effects of chronic ethanol treatment (CET) on muscarinic acetylcholine receptor (mAChR) binding properties were investigated via quantitative autoradiography in rats maintained on an ethanol‐containing liquid diet for 28 weeks and withdrawn from ethanol for 8 weeks before harvesting of tissues. Controls received an identical diet in which sucrose was substituted isocalorically for ethanol. Maximal binding of the radiolabeled mAChR antagonist quinuclidinyl benzilate ([ 3 H]QNB) was not reduced in hippocampal area CA1, dentate gyrus, neocortex, striatum, or thalamus, suggesting that CET results in no significant mAChR loss in these regions. Binding affinities of the cholinergic agonist carbachol to mAChRs were unaffected by CET in each of these regions, as determined by competitive displacement of [ 3 H]QNB labeling. These results suggest that CET‐induced functional deficits in brain cholinergic responses are not due to direct effects of CET on mAChR binding properties.