Abstract
ABSTRACT Administration of p-chlorophenylalanine (p-CPA), a brain serotonin (5-HT) depleting agent, induced a significant reduction in thyroid function as evaluated by the thyroid/serum ratio, 24 hour 131I uptake uptake and the 131I biological half-life. The iodo-amino acid composition of hydrolyzed thyroid tissue remained unchanged by the drug. The injection of thyrotrophin (TSH) to rats the endogenous TSH of which had previously been blocked with thyroxine, raised the plasma 131I and PB131I levels in both treated and control rats. The brain 5-HT concentration measured 24 hours following the last dose of p-CPA was markedly lowered by 50 mg/kg/day and 100 mg/kg/day. Cardiac 5-HT stores were only slightly depleted, while the thyroid 5-HT content remained unchanged. These results suggest a role of brain 5-HT depletion on the reduction of thyroid function caused by p-CPA. Some possible mechanisms are briefly discussed.
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