Mori M, Yamada M, Kobayashi S
First Department of Internal Medicine, Gunma University, School of Medicine, Maebashi, Japan.
Neuroendocrinology. 1988 Aug;48(2):153-9. doi: 10.1159/000125003.
We explored whether endogenous TRH in the hypothalamus produced a potential change in its receptors in the rat anterior pituitary. Thyroidectomy caused a progressive increase in the pituitary TRH binding with a concomitant increase in the blood TSH level. Injection of T4 prevented the increase in the pituitary TRH binding and the blood TSH level after thyroidectomy. The hypothalamic deafferentation and electrolytic lesions in the hypothalamic paraventricular nuclei led to a significant reduction in both the content of TRH in the hypothalamic median eminence and the blood TSH level, but they affected neither the number nor affinity constant of the pituitary TRH receptors in thyroidectomized rats. The present data provide evidence that TRH receptors in the anterior pituitary are profoundly regulated by thyroid hormones, but not significantly by TRH in the hypothalamus in the rat.
我们探究了下丘脑内源性促甲状腺激素释放激素(TRH)是否会使其在大鼠垂体前叶中的受体产生潜在变化。甲状腺切除导致垂体TRH结合逐渐增加,同时血液中促甲状腺激素(TSH)水平升高。注射甲状腺素(T4)可防止甲状腺切除后垂体TRH结合及血液TSH水平升高。下丘脑去传入神经支配以及下丘脑室旁核的电解损伤导致下丘脑正中隆起处TRH含量及血液TSH水平显著降低,但对甲状腺切除大鼠垂体TRH受体的数量和亲和常数均无影响。目前的数据表明,大鼠垂体前叶中的TRH受体受甲状腺激素的深刻调节,但不受下丘脑TRH的显著影响。