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首页> 外文期刊>The European Journal of Neuroscience >Differential disinhibition of the neonatal hypothalamic- pituitary-adrenal axis in brain-specific CRH receptor 1-knockout mice.
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Differential disinhibition of the neonatal hypothalamic- pituitary-adrenal axis in brain-specific CRH receptor 1-knockout mice.

机译：在大脑特异性CRH受体1基因敲除小鼠中，新生儿下丘脑-垂体-肾上腺轴的差异性抑制作用。

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In the adult, corticotropin-releasing hormone (CRH) is the key mediator for the behavioural and neuroendocrine response to stress. It has also been hypothesized that, during postnatal development of the stress system, CRH controls the activity of the HPA axis and mediates the effects of early disturbances, e.g. 24 h of maternal deprivation. In the current study we investigated the function of specific brain corticotropin-releasing hormone receptor type 1 (CRHR1) subpopulations in the control of the HPA axis during postnatal development under basal conditions as well as after 24 h of maternal deprivation. We used two conditional CRHR1-deficient mouse lines which lack this receptor, either specifically in forebrain and limbic structures (Cam-CRHR1) or in all neurons (Nes-CRHR1). Basal circulating corticosterone was increased in Nes-CRHR1 mice compared to controls. Corticosterone response to maternal deprivation was significantly increased in both CRHR1-deficient lines. In the paraventricular nucleus, Cam-CRHR1 animals displayed enhanced CRH and decreased vasopressin expression levels. In contrast, gene expression in Nes-CRHR1 pups was strikingly similar to that in maternally deprived control pups. Furthermore, maternal deprivation resulted in an enhanced response of Cam-CRHR1 pups in the brain, while expression levels in Nes-CRHR1 mouse pups were mostly unchanged. Our results demonstrate that brainstem and/or hypothalamic CRHR1 contribute to the suppression of basal corticosterone secretion in the neonate, while limbic and/or forebrain CRHR1 dampen the activation of the neonatal HPA axis induced by maternal deprivation.
机译：在成年人中，促肾上腺皮质激素释放激素（CRH）是行为和神经内分泌对压力反应的关键介质。还假设在应激系统的产后发育过程中，CRH控制着HPA轴的活动并介导了早期干扰的影响，例如：产妇剥夺24小时。在当前的研究中，我们调查了基础条件下的产后发育以及母体剥夺24小时后，特定的大脑促肾上腺皮质激素释放激素受体1型（CRHR1）亚群在HPA轴控制中的功能。我们使用了缺少此受体的两条条件性CRHR1缺陷小鼠系，特别是在前脑和边缘结构（Cam-CRHR1）或所有神经元（Nes-CRHR1）中。与对照组相比，Nes-CRHR1小鼠的基础循环皮质酮增加。在两个CRHR1缺陷型品系中，皮质酮对母体剥夺的反应均显着增加。在室旁核中，Cam-CRHR1动物表现出增强的CRH和降低的血管加压素表达水平。相比之下，Nes-CRHR1幼崽的基因表达与母性剥夺的对照幼崽的基因表达极为相似。此外，母体剥夺导致大脑中Cam-CRHR1幼崽的反应增强，而Nes-CRHR1小鼠幼崽的表达水平基本不变。我们的研究结果表明，脑干和/或下丘脑CRHR1有助于抑制新生儿的基础皮质酮分泌，而边缘和/或前脑CRHR1则抑制了母体剥夺引起的新生儿HPA轴的激活。

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