Journal of Neuroscience, Vol 4, 2160-2172, Copyright © 1984 by Society for Neuroscience
Glucocorticoids stimulate adrenergic differentiation in cultures of migrating and premigratory neural crest
J Smith and M Fauquet
Glucocorticoid hormones stimulate catecholamine (CA) anabolism in a variety
of adrenergic derivatives of the neural crest. We describe work performed
to investigate the action of these steroids on the catecholaminergic
differentiation of neural crest cells themselves. Crest was taken from the
trunk level of 2-day quail embryos, before migration had begun, and was
cultured in vitro. Adrenergic differentiation, characterized by the ability
of the cultures to synthesize and store CA, was minimal and was not
improved when glucocorticoids were added to the medium. In contrast,
extensive adrenergic differentiation occurred when neural crest cells,
removed from the embryo 24 hr later, toward the end of their migratory
phase, were cultured with the sclerotomal component of the somite (their
immediate embryonic microenvironment). This process was considerably
stimulated by corticosteroids; the rate of conversion of [3H]tyrosine to
intracellular CA (norepinephrine, epinephrine, and dopamine) was 2 to 3
times higher in cultures exposed for 7 days to 10(-6) to 10(-7) M
hydrocortisone, corticosterone, or dexamethasone, and the diameter of the
dense-core vesicles seen in cell bodies and processes after permanganate
fixation was strikingly increased. The effect was specific for the
adrenergic phenotype in that acetylcholine synthesis by the cultures was
consistently unaffected by hormone treatment. We infer that glucocorticoids
do not trigger adrenergic differentiation, but that they selectively
enhance catecholaminergic properties in crest cells that have already been
exposed to an appropriate signal of another kind. This conclusion is
strengthened by the observation that glucocorticoids stimulated the
development of CA-producing cells from premigratory crest grown in the
presence of somites and notochord, postulated sources of factors initiating
adrenergic differentiation in the embryo. Although the intervention of
glucocorticoids in vivo at very early embryonic stages remains to be
established, our results indicate that neural crest derivatives would be
potentially responsive to these hormones as soon as the sympathetic ganglia
form.