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Neonatal mice received oral doses of monosodium glutamate (MSG) at levels of 0.25, 0.5m 1.0, 2.0, and 4.0 g/kg or aspartame at levels of 0.5, 1.0, 1.5, and 2.0 g/kg. Hypothalamic lesions were encountered at dose levels equal to or exceeding 0.5 g/kg (MSG) and 1.0 g/kg (aspartame). Aspartame administration resulted in a much smaller hypothalamic lesion than did equal dosages of MSG. Infant monkeys received MSG (1-4 g/kg) or aspartame (2 g/kg) by stomach tube. Hypothalamic morphology remained normal at both the microscopic and ultrastructural level. Thus, in contrast to the neonatal rodent, the neonatal primate is able to cope either metabolically or at the level of the blood-brain barrier with excessive amino acid loads.
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Reynolds et al. (1976) studied this question.
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