Ethanol administration to rats for 30 days resulted in a significant decrease (-28%; P< 0.05) in the density of mitochondrial benzodiazepine receptors (MBR) in the olfactory bulb. The reduction in [3H]PK 11195 binding persisted 24 hr after cessation of alcohol and had returned to normal values when measured 4 days later. Alterations were confined to this brain region and were not detected in the cerebral cortex, cerebellum or hippocampus. [3H]PK 11195 binding was elevated in the liver (100%; P<0.01), heart (43%; P< 0.01) and testis (27%; P<0.05) 30 days following ethanol consumption and this persisted for 1 and 4 days after abrupt withdrawal. A transitory decrease (-20%; P<0.05) in MBR density was observed in the adrenal gland following 30 days of alcohol ingestion, but disappeared during withdrawal. The alterations in these receptors may be relevant to the cellular damage or dysfunction induced by chronic exposure to ethanol.
Bibliographical noteFunding Information:
Acknowledgements-Thisw ork was supportedi n part by Grant 26-90 (to M.G.) from the Israel Institute for Psychobiology-the CharlesE . Smith Family Foundation. We thankR uthS ingerf or typinga nde ditingt hem anuscript. This study is submitted in partial fulfillment of the requirementsfo r the D.Sc. degreeo f M. Bidder at the Technion-IsraelI nstituteo f Technology.
ASJC Scopus subject areas