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The Journal of Neuroscience, February 1, 1999, 19(3):1062-1071

Regulation of Neurotrophin Receptor Expression by Retinoic Acid in Mouse Sympathetic Neuroblasts

Sean Wyatt1, Rosa Andres1, Hermann Rohrer2, and Alun M. Davies1

1 School of Biological and Medical Sciences, Bute Medical Buildings, University of St. Andrews, St. Andrews, Fife KY16 9AJ, Scotland, and 2 Max-Planck-Institut für Hirnforschung, Abteilung Neurochemie, D-60528 Frankfurt/Main, Germany

We have studied the effect of retinoic acid on the expression of the neurotrophin receptors trkA, trkC, and p75 by neuroblasts and neurons at different axial levels along the embryonic mouse paravertebral sympathetic chain. In dissociated cultures of sympathetic neuroblasts, retinoic acid inhibited the developmental increase in trkA mRNA expression and the developmental decrease in trkC mRNA expression that normally occurs in these cells but did not affect p75 mRNA expression. At higher concentrations, retinoic acid also increased the proliferation of sympathetic neuroblasts. After sympathetic neuroblasts became postmitotic, retinoic acid no longer affected receptor expression. Studies with retinoic acid receptor agonists and antagonists indicated that the effects of retinoic acid on neurotrophin receptor expression were mediated mainly by alpha  retinoic acid receptors, not beta  or gamma  receptors. The observation that alpha -antagonists increased trkA mRNA expression in intact sympathetic ganglion explants suggests that endogenous retinoic acid is a physiological regulator of trkA receptor expression.

Key words: retinoic acid; Trk receptor; p75 receptor; neurotrophin; sympathetic neuron; sympathetic neuroblast

Copyright © 1999 Society for Neuroscience  0270-6474/99/1931062-10$05.00/0




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