Abstract
During the preconvulsive phase the acetylcholine content of the brain increased to 150% after admn. of physostigmine salicylate and to about 60% after admn. of pentamethylene tetrazole. The acetylcholine content decreased about 30% after admn. of ammonium chloride. Convulsions were initiated with ammonium chloride only when the acetylcholine content of the brain previously returned to within normal limits. During convulsions the acetylcholine content gradually decreased. The nature of changes of the electrical activity of the brain during the preconvulsive phase depends on the convulsion-inducing agent and its mechanism of action on the brain. The convulsion equivalent in the eeg. is similar regardless of the nature of the convulsion-inducing agent. It is concluded that convulsions do not occur with brain acetylcholine content below normal limits. The factor initiating convulsions may or may not be acetylcholine. During convulsions the acetylcholine content of the brain decreases, probably due to inhibition of the synthesis of acetylcholine by a metabolite, e.g., ammonium ion. Convulsions are suspended when the acetylcholine content of the brain decreases significantly below normal limits.

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