Neonatal methylmercury poisoning in the rat: effects on development of peripheral sympathetic nervous system. Neuronal participation in methylmercury-induced cardiac and renal overgrowth.

The effects of neonatal CH3-Hg exposure on development and function of peripheral catecholaminergic synapses were examined by measuring tissue norepinephrine (NE) levels and turnover rates and cardiac biochemical responses to sympathetic reflex stimulation. In the rat, cardiac sympathetic neurotransmission normally develops towards the end of the first week postnatally; however, pups given CH3-Hg showed responses to sympathetic reflex stimulation as early as 2 days of age. The accelerated maturation of cardiac sympathetic effect was accompanied by initial enhancement of NE levels and turnover. This effect appeared to be specific to the heart, as kidney displayed subnormal NE levels in CH3-Hg-treated animals. Since neonatal CH3-Hg produces heart and kidney overgrowth, we examined the potential role of sympathetic input in altered tissue growth, utilizing chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Sympathectomy inhibited the early phase of renal overgrowth, suggesting that sympathetic nerves participate in the initial effect of CH3-Hg on this tissue; however, 6-OHDA did not influence later phases of renal enlargement nor did it alter the CH3-Hg-induced cardiac overgrowth. These results indicate that neonatal exposure to CH3-Hg alters the synaptic development of peripheral catecholamine neurons, which may play a role in some of the subsequent effects on tissue development.