Allosteric modulation of flunitrazepam binding to rat brain benzodiazepine receptors by methyl beta-carboline-3-carboxylate.
The inhibition of flunitrazepam (FNP) binding to rat brain benzodiazepine (BZ) receptors by methyl beta-carboline-3-carboxylate (MCC) was studied. Biphasic dissociation was observed for [3H]FNP and [3H]MCC in cerebral cortex, cerebellum, and hippocampus, although the dissociation of [3H]MCC was much faster. The dissociation rate of [3H]FNP was increased by MCC in the cerebellum, but was not altered in cerebral cortex or hippocampus. [3H]FNP binding stimulated by gamma-aminobutyric acid was enhanced in the presence of MCC in all three regions examined. These results indicate that MCC exerts these effects by interacting with allosteric sites that are different from the FNP recognition sites on the BZ receptors.
Chiu
T H
TH
Rosenberg
H C
HC
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002243:Carbolines / Q000494:pharmacology*; D005445:Flunitrazepam / Q000378:metabolism*; D007211:Indoles / Q000494:pharmacology*; D007700:Kinetics; D051381:Rats; D011963:Receptors, GABA-A / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002243:Carbolines; D007211:Indoles; D011963:Receptors, GABA-A; C026072:1-methyl-beta-carboline-3-carboxylic acid; D005680:gamma-Aminobutyric Acid; D005445:Flunitrazepam