Investigations into the release of acetylcholine from the cerebral cortex of the cat: Effects of amphetamine, of scopolamine and of septal lesions

Abstract

The acetylcholine (ACh) output from the cerebral cortex was investigated in cats transected at midpontine pretrigeminal level; in some of the cats the septum was also electrocoagulated. P]Amphetamine (2.5 mg kg i.v.) caused an increase in ACh output which was prevented by pretreatment with α-methyl-p-tyrosine and by the septal lesion. P]Scopolamine, either applied locally in the collecting cylinders (1 μg ml ), or administered intravenously (1 mg kg ), caused an increase in ACh output which was prevented by cortical undercutting and was reduced by septal lesion. P]These results support the hypothesis that amphetamine increases ACh output through the release of catecholamines from adrenergic nerve endings; these in turn stimulate a cholinergic pathway which ascends to the cerebral cortex, and either originates from or passes through the septum. This pathway is also partly implicated in the increase in ACh output caused by scopolamine.