慢性应激对大鼠海马Akt/FKHRL1信号通路活性的影响

Activation of Akt/FKHRL1 Signaling Pathway after Chronic Stress in the Rat Hippocampus

探讨慢性应激对大鼠海马Akt/FKHRL1信号通路活性的影响，及其应激源特异性。将24只雄性SD大鼠随机分为心理应激组、束缚应激组和正常对照组（n=8）。用Western-blotting方法测定28天应激后海马Akt、FKHRL1蛋白含量及其磷酸化水平。结果表明，应激后三组大鼠海马磷酸化Akt、FKHRL1含量差异有统计学意义（p < 0.01；p < 0.001），束缚应激组低于正常对照组（p < 0.01）。提示慢性应激能导致海马磷酸化Akt、FKHRL1表达水平降低，但其影响程度与应激源特异性有关。

Introduction There is now a substantial body of evidence which suggests that chronic stress can increase susceptibility to disease such as depression and posttraumatic stress disorder. Chronic stress induces neuronal atrophy and death in the cortex as well as in the hippocampus. The proto-oncogene protein kinase B (PKB)， also known as Akt， is a central player in a signaling pathway of which many components have been linked to cellular survival. Akt as well as of its downstream targets Forkhead t