ACTIONS OF BENZODIAZEPINE AND BETA-CARBOLINE DERIVATIVES ON GAMMA-AMINOBUTYRIC ACID-ACTIVATED CL- CHANNELS RECORDED FROM MEMBRANE PATCHES OF NEONATAL RAT CORTICAL-NEURONS IN CULTURE

  • 1 December 1987
    • journal article
    • research article
    • Vol. 243  (3) , 1195-1201
Abstract
Using the patch-clamp, single-channel recording technique, the authors determined conductance and kinetics of .gamma.-aminobutyric acid-activated Cl- channels recorded from membrane patches excised from neonatal rat cortical neurons in primary culture. The anxiolytic benzodiazepine flunitrazepam increased the channel opening frequency, but it did not change conductance or channel opening burst duration. The anxiogenic compound methyl-6,7-dimethoxy-4-ethyl-.beta.-carboline-3-carboxylate decreased .gamma.-aminobutyric acid-activated Cl- channel opening frequency without changing conductance or opening duration. An increase and decrease in the number of channel bursts were elicited by flunitrazepam and methyl-6,7-dimethoxy-4-ethyl-.beta.-carboline-3-carboxylate, respectively. The effects of both drugs were antagonized by ethyl-8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo[1,5][1,4]-benzodiazepine-3-carboxylate (flumazenil), a benzodiazepine antagonist, which per se failed to modify Cl- channel kinetics and conductance.

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