Accelerated development of rat sympathetic neurotransmission caused by neonatal triiodothyronine administration
Lau, C.; Slotkin, T.A.
Journal of Pharmacology and Experimental Therapeutics 208(3): 485-490
1979
ISSN/ISBN: 0022-3565 PMID: 219177 Document Number: 146160
Effects of triiodothyronine (T3) on development of rat sympathetic nerve function in adrenal medulla and heart were evaluated by giving 0.1 mg/kg of T3 s.c. once daily for 9 days beginning the day after birth. Adrenal catecholamine (CA) depletion and heart ornithine decarboxylase induction were monitored after central stimulation of sympathetic pathways elicited by insulin-induced hypoglycemia. Insulin-induced depletion of catecholamines was absent in neonatal rats and the response matured by 8-10 days of age. In contrast, rats treated with T3 showed a significant adrenal response by 2 days of age and a totally mature response by 4-6 days. Despite the acceleration of the onset of functional sympathetic neurotransmission caused by T3, the adrenal medulla did not itself demonstrate enhanced development. In the heart, reflex sympathetic stimulation did not produce elevations of ornithine decarboxylase activity until 6 days of age in control rats, while rats treated with T3 showed a substantial cardiac ornithine decarboxylase response as early as 2 days. While heart weights of neonates treated with T3 were elevated during the first 10 days postnatally, there was subsequently a deficit in heart weight. In early development, transsynaptic neuronal input does not play the most important role in regulating adrenomedullary or cardiac development.