Abstract
Summary
Tryptophan deficiency did not affect either penetration or cerebral retention of reserpine-3H or tryptophan-5-hydroxylase activity of brain or liver. Administration of reserpine or acute cold exposure significantly increased tryptophan-5-hydroxylase activity in the brain in both sufficient and deficient rats while cold stress, in combination with another stress, was found to be an absolute requirement in decreasing hepatic hydroxylation of either tryptophan or phenylalanine. Cold exposed and reserpinized rats responded with a statistically significant depletion of both cerebral 5-HT and NE with concomitant deep sedation.
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