摘要
目的 探讨大鼠下丘脑神经元表达促肾上腺皮质激素释放激素(CRH)mRNA的蛋白激酶A(PKA)信号调控机制。方法 通过大鼠下丘脑脑片实验模型,运用Westernblot及逆转录多聚合酶链反应(RT PCR)技术,观察CRH激活下丘脑促肾上腺皮质激素释放激素Ⅰ型受体(CRH1R)后PKA信号通路的活性变化,及其与CRHmRNA表达的关系。结果 CRH可引起下丘脑脑片磷酸化PKA、磷酸化环腺苷一磷酸反应元件结合蛋白(CREB)及CRHmRNA含量明显增加,而CP -154526、H89可显著抑制磷酸化PKA、磷酸化CREB及CRHmRNA含量的增加。结论 在严重创伤应激反应中, CRH主要通过PKA途径实现对下丘脑神经元CRHmRNA表达的超短正反馈调节。
Objective To investigate protein kinase A (PKA) signal regulatory mechanism of expression of corticotropin-releasing hormone (CRH) mRNA, after CRH stimulated neuron of hypothalamic slices in rats in vitro.Methods After CRH corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro was stimulated, the relation between the changes of activity of PKA signal pathway and those of CRH mRNA expression was observed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting via the models of hypothalamic slices in rats.Results CRH may cause the remarkable increase in phosphorylated PKA (P-PKA), phosphorylated cyclic adenosine monophosphate response element-binding protein (P-CREB) and CRH mRNA content in hypothalamic slices in rats. However, CP-l54526 or H89 could have significant inhibitory effect on the synthesis of P-PKA, P-CREB and CRH.Conclusion PKA signal pathway in ultrashort positive feedback control of CRH secretion in hypothalamus in the stress is due to severe traumas.
出处
《中华神经外科疾病研究杂志》
CAS
2005年第2期141-144,共4页
Chinese Journal of Neurosurgical Disease Research
基金
国家重点基础研究专项经费资助"973"课题项目(G1999054201)
