THE EFFECT OF TERTIARY AND QUATERNARY ATROPINE ON CORTICAL ACETYLCHOLINE OUTPUT AND ON THE ELECTROENCEPHALOGRAM IN CATS

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Abstract
Application of diisopropylfluorophosphate (DFP) to the cortex of non-anesthetized cats resulted in a low output of acetylcholine (ACh) and the appearance of spikes. Intravenous administration of 1 mg/kg atropine sulphate increased ACh output threefold and caused high voltage electroencephalographic (EEG) patterns. While atropine methylbromide given intravenously was 10–20 times less effective than atropine sulphate in producing high voltage EEG, it was only 2–4 times less active in increasing ACh output. Small quantities (0.2 μg/ml) of atropine locally applied also increased ACh output without producing high voltage EEG, but the spikes previously present disappeared. Acetylcholine applied locally following DFP also abolished the spikes. It is concluded that atropine raises ACh output by a direct action on the area of ACh release, independently of EEG effects, and that the site on which cholinergic blocking agents act to raise ACh output is more accessible from the bloodstream than the site responsible for the EEG effects. The exact mechanism by which atropine increases ACh output could not, however, be established.

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