Abstract
Oral administration of either choline or physostigmine to rats stimulated the metabolism of dopamine in brain. Treatment of rats with an acetylcholine receptor blocker (atropine) or an inhibitor of acetylcholine synthesis [4-(1-naphthylvinyl) pyridine] antagonized the choline-induced increase in dopamine metabolism. In contrast to its effect on the choline-induced increase in dopamine metabolism, 4-(1-naphthylvinyl) pryridine did not prevent the increase induced by physostigmine. These results indicate that oral administration of choline augments central cholinergic function, and suggest that the mechanism involves stimulation of the rate of synthesis and release of acetylcholine.
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