RT Journal Article
SR Electronic
T1 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.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 1195
OP 1201
VO 243
IS 3
A1 Vicini, S
A1 Mienville, J M
A1 Costa, E
YR 1987
UL http://jpet.aspetjournals.org/content/243/3/1195.abstract
AB 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.