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Allosteric Modulation of Flunitrazepam Binding to Rat Brain Benzodiazepine Receptors by Methyl β‐Carboline‐3‐Carboxylate
Author(s) -
Chiu Ted H.,
Rosenberg Howard C.
Publication year - 1985
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1985.tb07145.x
Subject(s) - allosteric regulation , flunitrazepam , cerebellum , chemistry , dissociation (chemistry) , receptor , allosteric modulator , gabaa receptor , benzodiazepine , cerebral cortex , hippocampus , neuroscience , agonist , pharmacology , biophysics , biochemistry , biology
The inhibition of flunitrazepam (FNP) binding to rat brain benzodiazepine (BZ) receptors by methyl β‐carboline‐3‐carboxylate (MCC) was studied. Biphasic dissociation was observed for [ 3 H]FNP and [ 3 H]MCC in cerebral cortex, cerebellum, and hippocampus, although the dissociation of [ 3 H]MCC was much faster. The dissociation rate of [ 3 H]FNP was increased by MCC in the cerebellum, but was not altered in cerebral cortex or hippocampus. [ 3 H]FNP binding stimulated by γ‐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.