The effect of benzodiazepines and β-carbolines on gabastimulated chloride influx by membrane vesicles from the rat cerebral cortex

• Published in: Biochemical and biophysical research communications Vol. 141; no. 1; pp. 1 - 6
• Main Authors: Obata, Takaaki, Yamamura, Henry I.
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 26.11.1986
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/S0006-291X(86)80325-4

Benzodiazepine agonists such as diazepam, flunitrazepam and clonazepam enhanced GABA (30 μM )-stimulated 36C1 − uptake in membrane vesicles from the rat cerebral cortex. The rank order of potencies was flunitrazepam > diazepam = clonazepam. β-Carboline-3-carboxylate esters β-CCM,β-CCE and DMCM inhibited GABA-stimulated 36Cl − uptake. The rank order of inhibitory potencies was DMCM > β-CCM > β-CCE. The benzodiazepine antagonist Ro15-1788 antagonized the enhancement of flunitrazepam and the inhibition of DMCM on GABA-stimulated 36Cl − uptake in a competitive inhibitory manner. These results suggest that benzodiazepine receptors regulate GABA-stimulated 36Cl − uptake and there is a functional coupling between the GABA and benzodiazepine receptors, and chloride channels in membrane vesicles from the rat cerebral cortex.