Abstract
Thyroid hormone has been shown experimentally to affect cellular ion fluxes. For example, thyroid hormone-induced modulation has been described of cellular sodium current (I Na), inward rectifying potassium current (IKir) and sodium pump (Na, K-ATPase) and of calcium pump (Ca 2+-ATPase) activities. Certain of these actions appear to reflect nongenomic mechanisms of hormone action that are initiated at the plasma membrane receptor for iodothyronines described on integrin αvβ3. One such action is the recent demonstration of enhancement by the hormone of I Na in neurons. Nongenomic actions of thyroid hormone initiated at the plasma membrane may be specifically inhibited by tetraiodothyroacetic acid (tetrac), a deaminated thyroid hormone analogue. Important behavioral changes are associated with clinical states of excessive or deficient thyroid function. The molecular basis for these changes has not been established. It is proposed that nongenomic actions of thyroid hormone in neurons—such as that on sodium current—underlie certain of these behaviors. The contribution of such nongenomic actions of the hormone to animal behavioral paradigms possibly relevant to thyroid hormone actions in human subjects may be tested in vivo with tetrac.
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