The Release 'in vivo' of (H3) Acetylcholine from Cat Caudate Nucleus and Cerebral Cortex by Atropine, Pentylenetetrazol, K(+)-Depolarization and Electrical Stimulation.

摘要

In the present experiments, the resting and stimulus evoked release of (H3) acetylcholine from the caudate nucleus, the cerebral cortex, and the cerebellar cortex into the perfusate of the push-pull cannula was studied in the unanesthetized, midpontine, pretrigeminally transected cat following infusion at the push-pull site of (H3) choline. Separation of the metabolites in the perfusate revealed that after 20 minutes approximately 20% of the recovered radioactivity in the sample was in a lipid fraction, about 10% was found to be phosphorylcholine and around 3% was observed to be incorporated into acetylcholine. The rest of the recovered radioactivity remained as choline. Electrical stimulation applied directly to the caudate nucleus, local potassium depolarization, atropine and pentylenetetrazol were all observed to result in a significant and stimulus dependent increase in the levels of (H3) acetylcholine, but not (H3) choline or (C14) urea in the effluent of the push-pull cannula located in the caudate nucleus. A similiar release of newly synthesized (H3) acetylcholine was observed following atropine and potassium stimulation in the cerebral but not the cerebellar cortex. The specificity of this evoked increase in the levels of (H3) acetylcholine is substantiated by obtaining the release with stimuli having different modes of action, by the absence of stimulus evoked changes in the levels of other water-soluble elements found in the perfusate and by absence of an observable release of (H3) acetylcholine in perfusion experiments involving the cerebellum, a tissue not thought to have strong cholinergic innervation.