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© 1991 Medical Council on Alcohol

research-article

ETHANOL-INDUCED ALTERATIONS IN THE FUNCTION OF CEREBRAL GABAA RECEPTOR COMPLEX: EFFECT ON GABA-DEPENDENT 36Cl– INFLUX INTO CEREBRAL MEMBRANE VESICLES

TSUYOSHI UEHA and KINYA KURIYAMA*

Department of Pharmacology, Kyoto Prefectural University of Medicine Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto 602, Japan

*Author for correspondence.

Received 6 August 1990; first review notified 10 September 1990; Effect of addition in vitro of ethanol on the functions of the GABAA receptor complex was investigated using synaptic membrane preparation obtained from mouse brain. Ethanol (50–200 mM) had no significant effect on the specific bindings of [3H]muscimol to GABAA receptor and [3H]flunitrazepam to benzodiazepine receptor in cerebral particulate preparations. However, ethanol induced an inhibition of [3H]TBOB binding to Cl– channel and a suppression of flunitrazepam-induced enhancement of [3H]muscimol binding and of salsolinol-induced accentuation of [3H]flunitrazepam binding to cerebral particulate fraction. In contrast, ethanol facilitated GABA-dependent 36Cl– influx but eliminated the stimulatory effects of flunitrazepam and salsolinol on GABA-dependent 36Cl– influx into cerebral membrane vesicles. These results suggest that ethanol may facilitate the function of GABA-gated chloride channel in spite of inducing deteriorations of antagonist binding capacity of chloride channel as well as of the functional coupling between GABAA receptor and benzodiazepine receptor in the brain.


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