RECENT work from this laboratory has documented the initial expression of the noradrenergic phenotype in autonomie neuroblasts of the rat embryo in vivo. Tyrosine hydroxylase (T-OH) (rate-limiting enzyme in catecholamine biosynthesis)1, dopamine-β-hydroxylase (DBH) (which converts dopamine to noradrenaline) and the catecholamine (CA) transmitters appear simultaneously in sympathetic ganglion primordia at 11.5 days of gestation 2,3. In addition, these noradrenergic characters transiently appear in a population of presumptive neuroblasts within the primitive gut mesenchyme2,3. The noradrenergic gut neuroblasts appear at 11 .5 days and increase in numbers over the ensuing 24 hours. Subsequently, however, numbers decrease progressively so that by 14.5 days of gestation virtually no cells exhibiting noradrenergic traits are detectable2,3. Elucidation of the fate of these neuroblasts may help define mechanisms influencing neuronal phenotypic expression and/or the factors which govern selective neuronal death during ontogeny. In this report we show that treatment with the trophic protein macromolecule, nerve growth factor (NGF), increases the number of catecholamine (CA)-fluorescent cells and delays the ontogenetic disappearance of CA from the gut.
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