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 The changes in sensitivity observed in the ethanol withdrawn rats were reproduced by acute and chronic reserpinization.