Effect of ethanol on the cyclic AMP system in rat brain.

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Abstract
The effects of alcohol on adenylate cyclase and phosphodiesterase activity in vitro, and on cyclic[c]AMP, ATP and adenosine levels in vivo were studied in male Sprague-Dawley rats (200-250 g). Alcohol in lethal concentrations (1.732 M) inhibited adenylate cyclase activity in in-vitro preparations of all brain areas. Lower, but still lethal, concentrations increased adenylate cyclase activity in the cerebellum and cerebral cortex while the activity in the brain stem was not changed. Sublethal concentrations (less than 0.108 M) did not affect adenylate cyclase activity in preparations from any brain area. Phosphodiesterase activity, determined at 2 different substrate concentrations, was unchanged by alcohol (0.025-0.346 M) in any brain area. Concentrations of cAMP, ATP and adenosine were determined in the hind brain of control and alcohol-treated animals which were decapitated and the brain enzymes then inactivated by microwave irradiation. Oral administration of alcohol in a 15% (vol/vol) solution (5 ml of solution/kg of body weight) 1 h before decapitation significantly inhibited the rise of cAMP levels in pons medulla oblongata and cerebellum (P < .025). The decline of ATP levels after decapitation was slower in alcohol-treated rats than in control animals (P < .05). Decapitation induced an increase of adenosine levels in the hind brain of control animals but not in the alcohol-treated rats (P < .005). Alcohol affects the cAMP system indirectly, probably through its effect on neurotransmitter release or on adenosine formation.