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Thyroid Factor

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^ The actions of TRH on a thyrotroph. TRH 8 b binds to membrane receptors, which are cou pled to phospholipase C (PLC) by G proteins (Gq). PLC hy-drolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) in the plasma membrane, generating inositol trisphosphate (IP3) and di-acylglycerol (DAG). IP3 mobilizes intracellular stores of Ca2+. The rise in Ca2+ stimulates TSH secretion. Ca2+ and DAG activate protein kinase C (PKC), which phosphorylates proteins (P proteins) involved in stimulating TSH secretion and the expression of the genes for the a and P subunits of TSH.

The rise in cytosolic Ca2+ and the increase in DAG activate PKC in thyrotrophs. PKC phosphorylates proteins that are in some way involved in stimulating TSH secretion.

TRH also stimulates the expression of the genes for the a and P subunits of TSH (see Fig. 32.8). As a result, the amount of mRNA for the a and P subunits is maintained in the thy-rotroph and the production of TSH is fairly constant.

Thyroid Hormones and TSH Synthesis and Secretion.

The thyroid hormones exert a direct negative-feedback effect on TSH secretion. For example, when the blood concentration of thyroid hormones is high, the rate of TSH secretion falls. In turn, the stimulatory effect of TSH on the follicular cells of the thyroid is reduced, resulting in a decrease in T4 and T3 secretion. However, when the circulating levels of T4 and T3 are low, their negative-feedback effect on TSH release is reduced and more TSH is secreted from thyrotrophs, increasing the rate of thyroid hormone secretion. This control system is part of the hypothalamic-pituitary-thyroid axis (Fig. 32.9).

The thyroid hormones exert negative-feedback effects on both the hypothalamus and the pituitary. In the hypothalamic TRH-secreting neurons, thyroid hormones reduce TRH mRNA and TRH prohormone to decrease TRH re

Hypothalamus

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Essentials of Human Physiology

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