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Published July 1983 | Published
Journal Article Open

Tyrosine hydroxylase activity decreases with induction of cholinergic properties in cultured sympathetic neurons

Abstract

Establishment of transmitter phenotype is an essential step in neuronal development. Studies on rat sympathetic neurons both in vivo and in vitro have provided evidence that mature cholinergic sympathetic neurons arise from previously noradrenergic neurons. Cultured rat superior cervical ganglion neurons can be influenced by their environment to remain noradrenergic, to acquire dual transmitter function, or to become predominantly cholinergic. Several other neuronal traits, such as a variety of surface molecules and released proteins, change simultaneously with levels of catecholamine and acetylcholine production, suggesting that various components of transmitter phenotype are regulated in concert. In this report, tyrosine hydroxylase levels are compared in neurons cultured under noradrenergic, dual function, or cholinergic conditions. Both enzyme activity in cell extracts and immunocytochemical staining were measured. These methods showed significantly less tyrosine hydroxylase enzyme activity and immunoreactive material in cholinergic cultures compared to noradrenergic and dual function cultures. These data support the interpretation that a switch in transmitter status from noradrenergic to cholinergic has occurred. This interpretation contrasts with that of Iacovitti et al. (Iacovitti, L., T. H. Joh, D. H. Park, and R. P. Bunge (1981) J. Neurosci. 1: 685–690), who conducted their experiments under critically different culture conditions.

Additional Information

© 1983 Society for Neuroscience. For the first six months after publication SfN's license will be exclusive. Beginning six months after publication the Work will be made freely available to the public on SfN's website to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). Received December 13, 1982; Revised February 25, 1983; Accepted March 1, 1983. This work was supported by grants from the National Institute of Neurological and Communicative Disorders and Stroke. E. W. is a predoctoral trainee of the National Institute of General Medical Sciences and P. H. P. is a Rita Allen Foundation Scholar and a McKnight Foundation Neuroscience Development Awardee. We wish to thank Doreen McDowell, Geraldine Spencer, Allison Doupe, and Shirley Wilson for assistance with the cell cultures and with the preparation of the manuscript. We also thank Tom Jessell for advice on photography. Antiserum against tyrosine hydroxylase was a gift from J. Thibeault.

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