Iodothyronine homeostasis in rat brain during hypo- and hyperthyroidism.

Thyroid hormones are concentrated, retained, and metabolized in discrete neural systems in rat brain. To determine how iodothyronine requirements of brain compare with those of other thyroid hormone-dependent tissues, we measured effects of chronic thyroid hormone deficiency or excess on brain iodothyronine economy and particularly on the intracerebral rate of triiodothyronine formation from thyroxine. The results demonstrate that despite extremes of thyroxine availability, brain thyroxine and triiodothyronine concentrations and brain triiodothyronine production and turnover rates are kept within narrow limits. Adjustments in the activity of both brain and liver help to maintain these relatively stable conditions. Following thyroidectomy, fractional rates of triiodothyronine formation from thyroxine decrease to low levels in liver, whereas they increase markedly in brain; exactly the opposite direction of change occurs in brain and liver during hyperthyroidism. These responses suggest that brain iodothyronine homeostasis is important for the function of the whole organism. Because signs of nervous system dysfunction develop in hypothyroid and hyperthyroid individuals, it is possible that even relatively small deviations of brain iodocompound economy can produce significant changes in behavior and autonomic nervous system function.