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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Repeated stress impairs endocannabinoid signaling in the paraventricular nucleus of the hypothalamus.
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Repeated stress impairs endocannabinoid signaling in the paraventricular nucleus of the hypothalamus.

机译：反复应力损害下丘脑的椎间盘内核中的内胆蛋白信号传导。

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摘要

Endocannabinoids (eCBs) are ubiquitous retrograde signaling molecules in the nervous system that are recruited in response to robust neuronal activity or the activation of postsynaptic G-protein-coupled receptors. Physiologically, eCBs have been implicated as important mediators of the stress axis and they may contribute to the rapid feedback inhibition of the hypothalamic-pituitary-adrenal axis (HPA) by circulating corticosteroids (CORTs). Understanding the relationship between stress and eCBs, however, is complicated by observations that eCB signaling is itself sensitive to stress. The mechanisms that link stress to changes in synaptic eCB signaling and the impact of these changes on CORT-mediated negative feedback have not been resolved. Here, we show that repetitive immobilization stress, in juvenile male rats, causes a functional downregulation of CB(1) receptors in the paraventricular nucleus of the hypothalamus (PVN). This loss of CB(1) receptor signaling, which requires the activation of genomic glucocorticoid receptors, impairs both activity and receptor-dependent eCB signaling at GABA and glutamate synapses on parvocellular neuroendocrine cells in PVN. Our results provide a plausible mechanism for how stress can lead to alterations in CORT-mediated negative feedback and may contribute to the development of plasticity of HPA responses.
机译：Endocannaboids（ECBS）是神经系统中的逆行逆行信号分子，其响应于鲁棒神经元活性或突触后G蛋白偶联受体的激活而征收。生理学上，ECBS被认为是应力轴的重要介质，并且它们可以通过循环皮质类固醇（皮质）来促进下丘脑 - 垂体 - 肾上腺轴（HPA）的快速反馈抑制。然而，了解压力和欧洲央行之间的关系，通过观察结果，ECB信号传导本身对压力敏感。突触ECB信号传导中的压力和这些变化对皮质介导的负反馈的影响的机制尚未得到解决。在此，我们表明，在幼牙大鼠中，重复的固定应力导致下丘脑（PVN）中CB（1）受体的功能下调。该损失需要激活基因组糖皮质激素受体的CB（1）受体信号传导损失在PVN中的GABA和谷氨酸突突突突中损害活性和受体依赖性ECB信号传导。我们的结果提供了一种合理的机制，用于如何导致皮质介导的负反馈中的改变，并且可能有助于开发HPA反应的可塑性。

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