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Published August 1988 | public
Journal Article

Basic FGF Induces Neuronal Differentiation, Cell Division, and NGF Dependence in Chromaffin Cells: A Sequence of Events in Sympathetic Development


To define further the molecules that control sympathoadrenal differentiation, we have investigated the effects of FGF, NGF, and glucocorticoid on cultured neonatal rat adrenal chromaffin cells. Basic FGF (bFGF), like NGF, induces cell division and neurite outgrowth from these cells. Dexamethasone inhibits neuronal differentiation but not proliferation induced by bFGF Unlike NGF, bFGF will not support the survival of chromaffin cell-derived sympathetic neurons. However, bFGF induces a dependence on NGF The overlapping but distinct responses to NGF and bFGF may underlie a sequence of events in sympathetic differentiation. bFGF (or another factor) may act locally in developing ganglia to stimulate mitotic expansion and initial axon outgrowth. Subsequent survival and maturation are then controlled by NGF, which is provided by peripheral targets of innervation. In the adrenal gland, glucocorticoids may permit bFGF to amplify the chromaffin population, while preventing neuronal differentiation.

Additional Information

© 1988 by Cell Press. Received 21 March 1988, Revised 23 May 1988. The authors wish to express great thanks to Paul H. Patterson for his advice, support, and enthusiasm throughout the course of this work and for his critical comments on this manuscript. We thank Doreen McDowell for the preparation of tissue culture media and collagen and Josette Carnahan for the preparation of 7S NGF. We would also like to thank Forrest Fuller (California Biotech, Inc.). Gera Neufeld (UCSF), and Alan Williams (Oxford University) for the provision of the recombinant human bFGF, purified bovine bFGF, and the OX-7 hybridoma line, respectively. D. L. S. is supported by an NIH Training Grant, and N. K. M. is a recipient of an NSF Graduate Fellowship. This work is supported by grants from the NINCDS and the McKnight Foundation to Paul H. Patterson and by NIH grant No. RO1 NS23476.01 and Searle Scholar and NSF Presidential Young Investigator awards to D. J. A.

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