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首页> 外文期刊>The European Journal of Neuroscience >Brief treatment with the glucocorticoid receptor antagonist mifepristone normalizes the reduction in neurogenesis after chronic stress.
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Brief treatment with the glucocorticoid receptor antagonist mifepristone normalizes the reduction in neurogenesis after chronic stress.

机译：糖皮质激素受体拮抗剂米非司酮的简短治疗可将慢性应激后神经发生的减少恢复正常。

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摘要

In rodents, stress suppresses adult neurogenesis. This is thought to involve activation of glucocorticoid receptors in the brain. In the present study, we therefore questioned whether glucocorticoid receptor blockade by mifepristone can normalize the effects of chronic stress on adult neurogenesis. Rats received mifepristone on the last 4 days of a 21-day chronic unpredictable and inescapable stress regimen. Neurogenesis was analysed by stereological quantification of adult-generated cell survival (bromodeoxyuridine), young neuronal survival (doublecortin) and cell proliferation (Ki-67). The results show that only 4 days of mifepristone treatment normalized the stress-induced reductions in neurogenesis. Importantly, mifepristone by itself had no effect on neurogenesis. We conclude that, contrary to other compounds interfering with the effects of chronic stress on neurogenesis, like antidepressants, the normalizing effects of mifepristone on neurogenesis are rapid and particularly potent in a high stress environment. This neurogenic action of mifepristone could potentially contribute to its clinical mechanism of action.
机译：在啮齿动物中，压力会抑制成年神经发生。人们认为这涉及大脑中糖皮质激素受体的激活。因此，在本研究中，我们质疑米非司酮对糖皮质激素受体的阻断作用能否使慢性应激对成人神经发生的影响正常化。在为期21天的慢性不可预测且不可避免的压力治疗方案的最后4天，大鼠接受了米非司酮。通过成年细胞存活率（溴脱氧尿苷），年轻神经元存活率（doublecortin）和细胞增殖（Ki-67）的立体定量分析来分析神经发生。结果表明，米非司酮治疗仅4天即可使压力诱导的神经发生减少正常化。重要的是，米非司酮本身对神经发生没有影响。我们得出结论，与其他化合物（如抗抑郁药）干扰其他慢性应激对神经发生的作用相反，米非司酮对神经发生的正常作用是迅速的，在高压力环境下尤其有效。米非司酮的这种神经源性作用可能有助于其临床作用机制。

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