QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (21) Citing Articles via Google Scholar Google Scholar Articles by Henion, P. D. Articles by Landis, S. C. Search for Related Content PubMed PubMed Citation Articles by Henion, P. D. Articles by Landis, S. C.

 Previous Article  |  Next Article 

Journal of Neuroscience, Vol 12, 3818-3827, Copyright © 1992 by Society for Neuroscience

ARTICLE

Developmental regulation of leucine-enkephalin expression in adrenal chromaffin cells by glucocorticoids and innervation

PD Henion and SC Landis
Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44129.

Most catecholaminergic cells derived from the sympathoadrenal lineage of the neural crest contain one or more neuropeptides. Although a great deal is known about the development and regulation of catecholaminergic properties in these cells, relatively little is known about the developmental control of their neuropeptidergic properties. We have investigated the possible role of glucocorticoids and preganglionic innervation in the regulation of leucine-enkephalin (L-Enk) expression in cultures of embryonic and neonatal adrenal chromaffin cells and in mature chromaffin cells in vivo. Exposure of embryonic and neonatal chromaffin cells to the synthetic glucocorticoid dexamethasone increases L-Enk content. Neonatal chromaffin cells grown in medium containing elevated levels of potassium to mimic depolarization also exhibited increased L-Enk levels. The depolarization-induced increase in L-Enk was selectively inhibited by treatment with the enkephalin analog [D-Ala, d-Leu]-enkephalin to mimic the enkephalinergic component of the preganglionic innervation. Denervation of the adrenal gland in vivo resulted in a dramatic increase in L-enk expression that could be partially mimicked by selectively blocking enkephalinergic transmission with administration of the opiate receptor antagonist naloxone. Taken together with the developmental time course and pattern of L-Enk expression in vivo, our results suggest that glucocorticoids and the preganglionic innervation regulate the developmental expression of this peptide in adrenal chromaffin cells and therefore participate in the generation of the mature neurochemical phenotypes present in the adrenal medulla. Further, in adult chromaffin cells similar factors appear to regulate the expression of L-Enk, which could in turn participate in physiological responses to stress.

This article has been cited by other articles:

				S. R. Bornstein, H. Tian, A. Haidan, A. Bottner, N. Hiroi, G. Eisenhofer, S. M. McCann, G. P. Chrousos, and S. Roffler-Tarlov Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo PNAS, December 19, 2000; 97(26): 14742 - 14747. [Abstract] [Full Text] [PDF]

				P. Henion and J. Weston Timing and pattern of cell fate restrictions in the neural crest lineage Development, January 11, 1997; 124(21): 4351 - 4359. [Abstract] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help