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Published 1989 | public
Journal Article

Role of glucocorticoids in the chromaffin-neuron developmental decision


Chromaffin cells and sympathetic neurons develop from a common neural crest-derived progenitor cell. The developmental fate of this cell differs depending upon whether it migrates to the sympathetic ganglion or to the adrenal gland primordium, suggesting that local environmental signals control its differentiation. Glucocorticoid (GC) is a good candidate for an important adrenal environmental signal. These steroids are known to regulate PNMT, an adrenal-specific enzyme. However, in vivo observations suggest that the adrenal microenvironment influences the phenotype of sympathoadrenal progenitor cells as early as E14.5, 2 days before PNMT is first expressed by developing chromaffin cells. Using cDNA probes, we find that GC receptor mRNA can be detected in the embryonic adrenal at least one full day before the initial appearance of PNMT mRNA. This observation is compatible with the idea that the apparent early influence of the adrenal microenvironment reflects the action of GC on progenitors which have migrated into this environment. In support of this, we show that similar influences can be exerted by GC on PC12 cells, which contain GC receptor mRNA but do not express or induce PNMT mRNA. Taken together, these data suggest that other factors in addition to the presence of the GC receptor may be necessary for the developmental appearance of PNMT expression.

Additional Information

© 1989 Pergamon Press. Received 14 December 1988, Revised 16 February 1989, Accepted 13 March 1989. This work was supported by NIH grant no. R01 NS23476-01, and NSF Presidential Young investigator and Searle Scholar Awards to D.J.A. A.M. is supported by NIH predoctoral training grant no. 5-T32-GM07737. We thank Paul Patterson and Josette Carnahan for sharing their unpublished data with us and for helpful discussions, Dr Barry Kaplan for generously providing the bovine PNMT cDNA probe, and Dr Keith Yamamoto for his kind gift of the GCR cDNA probe.

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