Neurochemical alterations induced by manganese chloride in neonatal rats.

Male rats were exposed to manganese at doses of 1, 10, and 20 microg/g body weight/day from birth to day 24 post-partum. Animals were weighed and examined daily. The animals showed no visible signs of toxicity and exhibited normal weight gain. On day 25 the animals were killed by decapitation and the hypothalamic area and corpus striatum were removed and analyzed for several neurochemical components. Chronic manganese administration (10 and 20 microg/g) caused a significant reduction in the concentration of endogenous dopamine in the hypothalamic area. The concentration of endogenous norepinephrine in the hypothalamic area was unaffected at all levels of manganese administration. The depletion of dopamine induced by alpha-methyl-p-tyrosine was less in the hypothalamic area of chronic manganese-treated rats suggesting that dopamine turnover was reduced. No significant changes in neurochemical components occurred in the corpus striatum. Manganese at a dose of 20 microg/g caused a significant decrease in hypothalamic tyrosine hydroxylase activity and a significant increase in hypothalamic monoamine oxidase activity. The dosing regimen of 10 and 20 microg/g caused a significant elevation in tissue levels of manganese in both the hypothalamic area and corpus striatum. The results of this study indicate that minor alterations in the manganese content of the developing rat brain can lead to neurochemical alterations in specific brain regions.