INITIAL DEVELOPMENT OF THE NORADRENERGIC PHENOTYPE IN AUTONOMIC NEUROBLASTS OF THE RAT EMBRYO INVIVO

Initial development of the noradrenergic phenotype was defined in autonomic neuroblasts of the rat embryo in vivo. Adrenergic differentiation was documented by examining the appearance of the catecholamine (CA) biosynthetic enzymes tyrosine hydroxylase (T-OH), dopamine-.beta.-hydroxylase (DBH) and phenylethanolamine-N-methyltransferase (PNMT), and of the CA transmitters. Immunocytochemical and fluorescence histochemical methods were employed. None of these adrenergic traits were detectable in the neural crest itself or in the ventrally migrating crest cells. T-OH, DBH and CA simultaneously appeared at 11.5-12 days of gestation (27-30 somites) in neuroblasts aggregating to form the sympathetic ganglion primordia. Thereafter, fluorescence intensity and the number of noradrenergic cells progressively. T-OH, DBH and CA transiently appeared at 11.5 days in neuroblasts within the gut mesenchyme. The number of gut noradrenergic neuroblasts increased rapidly during the succeeding day, but thereafter decreased so that by 13.5 days only rare cells were encountered. There was striking synchrony in the appearance of noradrenergic characters in the ganglion anlage and gut, and in their disappearance in cells of the gut. PNMT, which synthesizes epinephrine, was undetectable in primitive ganglia or gut neuroblasts, suggesting that expression of the adrenergic phenotype is regulated in a manner different from that of the noradrenergic phenotype.