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首页> 外文期刊>The European Journal of Neuroscience >Early-life stress-induced anxiety-related behavior in adult mice partially requires forebrain corticotropin-releasing hormone receptor 1
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Early-life stress-induced anxiety-related behavior in adult mice partially requires forebrain corticotropin-releasing hormone receptor 1

机译：成年小鼠的早期生活应激诱导的焦虑相关行为部分需要前脑的促肾上腺皮质激素释放激素受体1

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摘要

Early-life stress may lead to persistent changes in central corticotropin-releasing hormone (CRH) and the CRH receptor 1 (CRHR1) system that modulates anxiety-related behavior. However, it remains unknown whether CRH-CRHR1 signaling is involved in early-life stress-induced anxiety-related behavior in adult animals. In the present study, we used conditional forebrain CRHR1 knockout (CRHR1-CKO) mice and examined the potential role of forebrain CRHR1 in the anxiogenic effects of early-life stress. As adults, wild-type mice that received unstable maternal care during the first postnatal week showed reduced body weight gain and increased anxiety levels in the open field test, which were prevented in stressed CRHR1-CKO mice. In the light-dark box test, control CRHR1-CKO mice were less anxious, but early-life stress increased anxiety levels in both wild-type and CRHR1-CKO mice. In the elevated plus maze test, early-life stress had only subtle effects on anxiety-related behavior. Moreover, early-life stress did not alter the basal home cage activity and gene expression levels of key hypothalamic-pituitary-adrenal axis regulators in adult wild-type and CRHR1-CKO mice, but enhanced neuroendocrine reactivity to acute immobilization stress in CRHR1-CKO mice. Our findings highlight the importance of forebrain CRHR1 in modulating some of the anxiogenic effects of early-life stress, and suggest that other neural circuits are also involved in the programming effects of early-life stress on anxiety-related behavior. Forebrain corticotropin-releasing hormone receptor 1 (CRHR1) may modulate the anxiogenic effects of early-life stress. Here we report that early-life stress-evoked anxiety-related behavior in adult mice can be partially prevented by postnatal deletion of CRHR1 in forebrain neurons. Moreover, in stressed animals, forebrain CRHR1 inactivation attenuates body weight loss during development and adulthood, and accelerates recovery to acute stress challenge.
机译：早期生活压力可能导致中枢促肾上腺皮质激素释放激素（CRH）和CRH受体1（CRHR1）系统持续变化，从而调节焦虑相关行为。然而，CRH-CRHR1信号是否参与成年动物的早期生活压力诱导的焦虑相关行为仍是未知的。在本研究中，我们使用条件性前脑CRHR1基因敲除（CRHR1-CKO）小鼠，并检查了前脑CRHR1在早期应激的焦虑产生中的潜在作用。成年后，在产后第一个星期接受母体护理不稳定的野生型小鼠在野外试验中显示出体重减轻和焦虑水平降低，而在应激的CRHR1-CKO小鼠中则可以预防。在明暗盒测试中，对照CRHR1-CKO小鼠的焦虑程度较小，但早期生活压力增加了野生型和CRHR1-CKO小鼠的焦虑水平。在高架迷宫测试中，早期生活压力对焦虑相关行为的影响很小。此外，成年野生型和CRHR1-CKO小鼠的早期生活压力并没有改变其基础家笼活动和关键下丘脑-垂体-肾上腺轴调节剂的基因表达水平，但增强了CRHR1-CKO对急性固定应激的神经内分泌反应性老鼠。我们的发现突出了前脑CRHR1在调节早期应激的某些焦虑产生作用中的重要性，并表明其他神经回路也参与了早期应激对焦虑相关行为的编程作用。前脑促肾上腺皮质激素释放激素受体1（CRHR1）可能会调节早期应激的焦虑作用。在这里我们报告说，成年小鼠的早期生活压力诱发的焦虑相关行为可以通过出生前脑神经元中CRHR1的出生后缺失而得到部分预防。此外，在压力较大的动物中，前脑CRHR1失活可减轻发育和成年期间的体重减轻，并加速其对急性压力挑战的恢复。

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