海马体向下丘脑的输入会抑制促甲状腺激素和促甲状腺激素释放激素的基因表达。

Hippocampal input to the hypothalamus inhibits thyrotrophin and thyrotrophin-releasing hormone gene expression.

作者信息

Shi Z X, Levy A, Lightman S L

机构信息

Neuroendocrinology Unit, Charing Cross and Westminster Medical School, London, UK.

出版信息

Neuroendocrinology. 1993 Apr;57(4):576-80. doi: 10.1159/000126409.

DOI:10.1159/000126409

PMID:8367025

Abstract

We have used in situ hybridization histochemistry to determine the effect of hippocampal-hypothalamic disconnection on hypothalamic thyrotrophin-releasing hormone (TRH) and anterior pituitary thyrotrophin beta subunit (TSH beta) transcripts in adult male CFY rats. Electrothermal lesions of the fornix pathway significantly increased TRH and TSH transcripts and increased circulating levels of triiodothyronine (T3). Fornix transection did not, however, prevent feedback regulation of TRH and TSH transcripts during exogenous T3-induced hyperthyroidism or propylthiouracil-induced hypothyroidism. Hippocampal inputs to the hypothalamus contribute to setting the basal activity of the thyroid axis, but do not mediate the feedback effects of T3.

摘要

我们运用原位杂交组织化学技术，来测定海马-下丘脑切断术对成年雄性CFY大鼠下丘脑促甲状腺激素释放激素（TRH）及垂体前叶促甲状腺激素β亚基（TSHβ）转录本的影响。穹窿通路的电热损伤显著增加了TRH和TSH转录本，并提高了循环中三碘甲状腺原氨酸（T3）的水平。然而，穹窿横断并未阻止在外源性T3诱导的甲状腺功能亢进或丙硫氧嘧啶诱导的甲状腺功能减退期间TRH和TSH转录本的反馈调节。下丘脑的海马输入有助于设定甲状腺轴的基础活性，但并不介导T3的反馈作用。