Control of Chromaffin Cell Development and Adrenomedullary Function in the Neonate

摘要

Neonatal administration of triiodothyronine (T3) accelerates the onset of sympatho-adrenomedullary neurotransmission function. To examine whether this reflected enhanced maturation of splanchnic innervation, the authors assessed retrograde transport of horseradish peroxidase. There was an increased number of labelled preganglionic neuronal cell bodies in the spinal cord of the hyperthyroid pups. Ultrastructural 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. Replication of the chromaffin cells was terminated prematurely in the T3 group, leading to significant reductions of mitotic index and overall cell numbers. As a functional consequence of these cellular deficits, ontogeny of adrenal catecholamine biosynthesis and storage was retarded. In neonates rendered hypothyroid by propylthiouracil, opposite effects on the maturation of the sympatho-adrenomedullary axis were observed, indicating an obligatory role of endogenous thyroid hormones in development of the chromaffin cells and their function. (Copyright (c) 1988 Alan R. Liss, Inc.).