Changes in receptor sensitivity of the cerebral cortex and liver during chronic ethanol ingestion and withdrawal.
The evidence was reviewed supporting the noradrenergic sub- and supersensitivity hypothesis of ethanol withdrawal pathogenesis. New data indicates that the cAMP generating system linked to noradrenergic receptor sensitivity is in a steady state in the brain during ethanol withdrawal since the cAMP levels were not different from controls in vivo. Propranolol blocking experiments indicated the beta-adrenergic receptor is a necessary link in the increased cAMP response induced by ethanol withdrawal. The changes in sensitivity observed in the ethanol withdrawn rats were reproduced by acute and chronic reserpinization.
D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic / Q000187:drug effects*; D013375:Substance Withdrawal Syndrome / Q000378:metabolism*
D011941:Receptors, Adrenergic; D011433:Propranolol; D000242:Cyclic AMP; D009638:Norepinephrine