You are here:
CONTROL OF CHROMAFFIN CELL DEVELOPMENT AND ADRENOMEDULLARY FUNCTION IN THE NEONATE
Citation:
Lau, C., L. Ross, AND T. Slotkin. CONTROL OF CHROMAFFIN CELL DEVELOPMENT AND ADRENOMEDULLARY FUNCTION IN THE NEONATE. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/D-90/085.
Description:
Neonatal administration of triodothyronine (T3) accelerates the onset of sympatho-adrenomedullary neurotransmission function. o examine whether this reflected enhanced maturation of splanchnic innervation, we assessed retrograde transport of horse radish peroxidase. here was an increased number of labelled preganglionic neuronal cell bodies in the spinal cord of the hyperthyroid pups. ltra-structural examination also revealed a corresponding increase of synapses in the adrenal medulla, and the activities of choline acetyltransferase, an enzyme marker for preganglionic terminals was also elevated. eplication of the chromaffin cells was terminated prematurely in the T3 group, leading to significant reductions of mitotic index and overall cell numbers. s a functional consequence of these cellular deficits, ontogeny of adrenal catecholamine biosynthesis and storage was retarded. n neonates rendered hypothyroid by propylthiouracll, opposite effects on the maturation of the syspatho-adrenomedullary axis were observed, indicating an obligatory role of endogenous thyroid hormones in development of the chromaffin cells and their function. he finding that precocious synaptic input impedes chromaffin cell development also suggested that specific CNS pathways might control adrenomedullary maturation. ndeed, neonatal chemical lesions in the spinal cord (6-hydroxydopamine) also advanced the onset of sympatho-adrenomedullary responses, and resulted in a preferential elevation of epinephrine in development adrenals; in contrast, lesions of spinal serotonergic neurons (5,7-dihydroxytryptamine) led to a preferential reduction of adrenal norepinephrlne. hese results suggest that central monoamlnergic neurons impose selective influences on the maturation of specific chromaffin cell types in the adrenal medulla.