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 15 45 2 6、H89可显著抑制磷酸化PKA、磷酸化CREB及CRHmRNA含量的增加。结论 在下丘脑离体脑片培养条件下,CRH可通过PKA途径实现对下丘脑神经元CRHmRNA的表达的超短正反馈调节。
Objective To investigate protein kinase A (PKA) signal regulatory mechanism of corticotropin-releasing hormone (CRH) mRNA expression, after CRH stimulated neuron of hypothalamic slices in rats in vitro. Methods After CRH stimulated corticotropin-releasing hormone type 1 receptor (CRH1R) of hypothalamic slices in rats in vitro, the changes of activity of PKA signal pathway and their relationship with CRH mRNA expression were observed by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting. 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 inhibition effects 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 due to severe traumas.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2005年第10期964-967,共4页
Journal of Third Military Medical University
基金
国家重点基础研究发展规划资助项目 ("973"项目 ) (G19990 54 2 0 1)~~