Effects of Adrenocorticotrophic Hormone, Cortisone Acetate, and 17-Hydroxycorticosterone-21-Acetate on Acetylcholine Metabolism

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Abstract
Prolonged admn. of ACTH in vivo increased the ability of brain to synthesize acetylcholine. This increase averaged 60% in hypophysectomized and nonoperated animals, and 20% in adrenalectomized rats on forced salt intake. Addition of ACTH to choline acetylase in vitro failed to increase the activity of the enzyme, suggesting that ACTH increases the synthesis of acetylcholine not through a direct action of the enzyme but mainly through an increased relative concn. of enzyme potentiators. The effect of ACTH in increasing acetylcholine synthesis depends on an adrenal and an extra-adrenal factor. Cortisone and Compound F did not fully duplicate the effects of ACTH on acetylcholine synthesis. Hypophysectomy resulted in an avg. decrease of 50% of the ability of brain to synthesize acetylcholine. Adrenalectomy did not impair the acetylcholine synthesis in animals with restricted activity. The activity of acetylcholine esterase was slightly increased after prolonged admn. of ACTH and cortisone, and hypophysectomy. The increase was questionable after a single injn. of ACTH, cortisone, and Compound F. The activity of the enzyme in vitro was not modified by the addition of the hormones in concns. of less than 0.5 mg./100 mg. of brain cortex and increased somewhat if added in concns. of 1 mg. and more. The acetylcholine content of brain approximated normal values in animals receiving prolonged admn. of the hormones and hypophysectomized animals. ACTH in vitro did not modify the sensitivity of effector cells to chemical stimuli (acetylcholine, K). Cortisone increased the sensitivity of effector cells to chemical stimuli.

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