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促甲状腺激素释放激素在后叶垂体中的调节。

Regulation of thyrotropin-releasing hormone in the posterior pituitary.

作者信息

Rondeel J M, Klootwijk W, Linkels E, van Haasteren G A, de Greef W J, Visser T J

机构信息

Department of Endocrinology and Reproduction, Erasmus University Faculty of Medicine and Health Sciences, Rotterdam, The Netherlands.

出版信息

Neuroendocrinology. 1995 Apr;61(4):421-9. doi: 10.1159/000126864.

Abstract

Although the presence of thyrotropin-releasing hormone (TRH) in the posterior pituitary (PP) was reported more than one decade ago, knowledge on its origin, regulation and functional significance is lacking. In the present study we investigated the regulation of TRH in the rat PP. Analysis by specific RIA, anion and cation exchange chromatography and reverse-phase HPLC showed that all TRH immunoreactivity in the PP is accounted for by authentic TRH. Induction of hyperthyroidism with thyroxine increased levels of TRH in the PP by 20%, whereas in methimazole-treated, hypothyroid rats the content decreased by 25% versus untreated, euthyroid controls. Food deprivation for 3 days increased levels by 35% and refeeding completely normalized TRH content again. Also 14-17 days after castration, TRH in the PP was increased by 25% while testosterone substitution prevented this increase. Castration did not affect proTRH mRNA levels in the hypothalamus. One week after adrenalectomy or daily subcutaneous dexamethasone injections, TRH content in the PP was not affected. Treatment with disulfiram, an inhibitor of the peptidylglycine alpha-amidating monooxygenase (PAM), reduced levels of TRH in the PP by 20%. ProTRH and PAM mRNA levels were not affected in the hypothalamus by this treatment. Since TRH in the PP has been suggested to play a role in prolactin (PRL) release, we determined the content of TRH in the PP during a 6-hour suckling stimulus that increased PRL levels in peripheral blood 30-fold. Whereas TRH in the median eminence increased by 35%, 6 h after the initiation of suckling, TRH levels in the PP remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

尽管十多年前就有报道称垂体后叶(PP)中存在促甲状腺激素释放激素(TRH),但其来源、调节机制及功能意义仍不清楚。在本研究中,我们对大鼠垂体后叶中TRH的调节进行了研究。通过特异性放射免疫分析、阴离子和阳离子交换色谱以及反相高效液相色谱分析表明,垂体后叶中所有的TRH免疫反应性均由真实的TRH所致。用甲状腺素诱导甲状腺功能亢进使垂体后叶中TRH水平升高20%,而用甲巯咪唑治疗的甲状腺功能减退大鼠,其含量与未治疗的甲状腺功能正常对照组相比降低了25%。禁食3天使TRH水平升高35%,重新喂食后TRH含量又完全恢复正常。同样,去势后14 - 17天,垂体后叶中的TRH升高了25%,而睾酮替代可阻止这种升高。去势并不影响下丘脑前促甲状腺激素释放激素(proTRH)的mRNA水平。肾上腺切除或每日皮下注射地塞米松一周后,垂体后叶中的TRH含量未受影响。用肽基甘氨酸α-酰胺化单加氧酶(PAM)抑制剂双硫仑治疗可使垂体后叶中TRH水平降低20%。这种治疗对下丘脑前促甲状腺激素释放激素和PAM的mRNA水平没有影响。由于垂体后叶中的TRH被认为在催乳素(PRL)释放中起作用,我们测定了在6小时哺乳刺激期间垂体后叶中TRH的含量,该刺激使外周血中PRL水平升高了30倍。尽管在开始哺乳6小时后,正中隆起处的TRH升高了35%,但垂体后叶中的TRH水平保持不变。(摘要截短于250字)

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