2474361

Genetic differences in coupling of benzodiazepine receptors to chloride channels.

Article date: 1989/6/19

PubMed ID: 2474361

Journal name: Brain research (ISSN: 0006-8993)

ABSTRACT

The affinity and density of [3H]flunitrazepam binding sites and the ability of flunitrazepam to augment GABA-activated chloride flux were determined using membrane vesicles prepared from cortex of long-sleep (LS, alcohol-sensitive), short-sleep (SS, alcohol-resistant) and individual heterogeneous stock (HS) mice. LS membranes were more sensitive than SS membranes to the effects of flunitrazepam (and ethanol) on chloride flux but did not differ in the binding of [3H]flunitrazepam. Likewise, individual HS mice displayed marked differences in enhancement of chloride flux by flunitrazepam, but little difference in binding of flunitrazepam. These results suggest that there is little genetic variation in the binding of benzodiazepines to receptors, but there is a marked diversity in the coupling of these receptors to chloride channels. This implies the existence of 'spare receptors' in LS and most HS mice, but not in SS mice. These findings also suggest that genetic differences in alcohol sensitivity in vivo may be related to coupling of benzodiazepine binding to chloride channel function.

This document is available from: http://directlinks.cc/files/muscimol/2474361.pdf

Author List: Harris R A, Allan A M

Publication Types: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

Substances mentioned in the article: Chloride Channels; Chlorides; Ion Channels; Membrane Proteins; Receptors, GABA-A; Muscimol; Ethanol; Flunitrazepam;

Mesh terms: Animals; Cerebral Cortex/drug effects; Chloride Channels; Chlorides/metabolism; Ethanol/pharmacology; Flunitrazepam/metabolism; Ion Channels/metabolism; Male; Membrane Proteins/metabolism; Mice/genetics; Muscimol/pharmacology; Receptors, GABA-A/drug effects; Sleep/drug effects;

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