The modulation of neurotransmitter synthesis by steroid hormones and insulin

• Published in: Brain research Vol. 190; no. 1; p. 67
• Main Authors: Schubert, D, LaCorbiere, M, Klier, F G, Steinbach, J H
• Format: Journal Article
• Language: English
• Published: Netherlands 19-05-1980
• Subjects: Acetylcholine - biosynthesis; Animals; Cell Line; Choline O-Acetyltransferase - metabolism; Cortodoxone - pharmacology; Dexamethasone - pharmacology; Dose-Response Relationship, Drug; Estradiol - pharmacology; Glucocorticoids - pharmacology; Hydrocortisone - pharmacology; Insulin - pharmacology; Nerve Growth Factors - pharmacology; Nerve Regeneration - drug effects; Neurotransmitter Agents - biosynthesis; Rats; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - enzymology; Testosterone - pharmacology; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 0006-8993
• DOI: 10.1016/0006-8993(80)91160-9

Glucocorticoids stimulate tyrosine hydroxylase activity and catecholamine synthesis, while markedly inhibiting acetylcholine synthesis and storage in the a clone of sympathetic nerve-like cells. Nerve growth factor enhances the effect of glucocorticoids on tyrosine hydroxylase. The steroid effect is specific for glucocorticoids, since 11-desoxycortisol, testosterone, and estradiol-17 beta do not reproduce the effects of hydrocortisone and dexamethasone. Concomitant with the shift in neurotransmitter synthesis, there is an increase in the mean diameter of intracellular dense core vesicles. In contrast to glucocorticoids, insulin increases the specific activity of choline acetyltransferase through the interaction with typical insulin receptors. Insulin does not, however, alter the morphology of the cells, nor does it block the morphological response of the cells to nerve growth factor.