CCK-8 modulates GABA-stimulated [3H]-flunitrazepam binding in vitro.
In membranes from rat cerebral cortex, cholecystokinin-8 (CCK-8) did not modulate basal [(3)H]-flunitrazepam binding at either 4 degrees C or 37 degrees C. At a concentration of 10(-6) M, CCK(-8) significantly decreased gamma-amino-butyric acid (GABA)-stimulated (10(-6) M) [(3)H]-flunitrazepam binding at 37 degrees C. Scatchard analyses suggest that the decreased GABA-stimulated binding might be due to a decrease in the affinity of benzodiazepine receptors rather than to a decrease of number of binding sites. The observed modulation of benzodiazepine receptors by CCK-8 in vitro might explain some of the functional interactions between CCK and benzodiazepine systems.
Faculty of Ecology, University of Forestry, Sofia, Bulgaria.
C
C
Hadjiivanova
S
S
Belcheva
I
I
Belcheva
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects* / Q000378:metabolism; D005445:Flunitrazepam / Q000378:metabolism*; D018757:GABA Modulators / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000187:drug effects / Q000378:metabolism*; D012844:Sincalide / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D018757:GABA Modulators; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D005445:Flunitrazepam; D012844:Sincalide