Abstract
Chronic ethanol consumption induces an increase in striatal adenylate cyclase enzymatic activity but is unable to further potentiate the dopamine stimulated production of cyclic-AMP. In striatal membranes obtained from chronic ethanol-treated rats, apomorphine exerts a more potent inhibition of [3H]spiperone binding when compared with controls, demonstrating that ethanol increases the affinity of the dopaminergic receptors associated with adenylate cyclase activity. In addition, GTP is unable to modify the agonist component of dopamine receptor in membrane exposed 'in vivo' to ethanol. Data are discussed in terms of a derangement of receptor-adenylate cyclase coupling system produced by chronic ethanol treatment.
Original language | English |
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Pages (from-to) | 187-192 |
Number of pages | 6 |
Journal | Neuroscience Letters |
Volume | 40 |
Issue number | 2 |
DOIs | |
Publication status | Published - Sep 30 1983 |
Keywords
- adenylate cyclase
- chronic ethanol
- dopaminergic receptors
- GTP
- rat
ASJC Scopus subject areas
- Neuroscience(all)