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Ethanol alters the adenosine receptor‐N i ‐mediated adenylate cyclase inhibitory response in rat brain cortex in vitro
Author(s) -
Bauché F.,
Bourdeaux-Jaubert A.M.,
Giudicelli Y.,
Nordmann R.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)80239-9
Subject(s) - adenylate kinase , adenosine , inhibitory postsynaptic potential , chemistry , in vitro , ethanol , cyclase , adenosine receptor , receptor , pharmacology , medicine , biochemistry , endocrinology , biology , agonist
It has been suggested that ethanol stimulates adenylate cyclase in vitro through an increased function of N s , the activitory component of adenylate cyclase. Because of the interaction of N s with N i , the adenylate cyclase inhibitory component, we have studied the effect of ethanol (0.05–0.2 M) on N i ‐mediated adenylate cyclase inhibition caused by the adenosine analog N 6 ‐phenylisopropyladenosine (N 6 ‐PIA) in brain cortical membranes. Ethanol did not alter N 6 ‐PIA binding to the adenosine R i ‐receptors, stimulated slightly basal adenylate cyclase activity but abolished adenylate cyclase inhibition due to N 6 ‐PIA, suggesting an effect of ethanol on the inhibitory coupling pathway. This was further supported by loss of the adenylate cyclase inhibitory response to GTP (10 −5 M). It thus seems that, besides its effect on the N s system, ethanol may also impair N i ‐mediated adenylate cyclase responses in rat cerebral cortex.