Abstract
The neonatal mouse was shown to share with the neonatal rat and kitten an initial inability to excrete the essential element manganese. In the mouse, it was shown that the blood-brain barrier against the metal is much less efficient postnatally than in the mature mouse. Varying the dietary concentration of manganese consumed by lactating mothers showed that the manganese concentration in the mother's milk tended to rise with that in the diet. The tissue manganese concentrations of both mothers and offspring, when plotted against the concentration of the metal in the diet, described straight lines with very low slopes: for relatively small increments of tissue concentration one needed large increments of dietary manganese. Only when massive dietary manganese levels were reached was there a sudden, marked increase in the tissues of both mothers and offspring. Under such dietary conditions, the offspring showed premature initiation of the metal's excretion. In view of the effects of chronic manganese poisoning on cerebral dopamine, appropriate measurements were initiated which, for the moment, have shown the following: that adult mice consuming diets containing massive amounts of manganese developed statistically significant elevations of cerebral dopamine.
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