BACKGROUND The involvement of microglia in neuroinflammatory responses has been extensively demonstrated. Recent animal studies have shown that exposure to either acute or chronic stress induces robust microglial activation in the brain. In the present study, we investigated the underlying mechanism of brain microglial activation by acute stress. METHODS We first looked at the spatial distribution of the noradrenaline (NA)-synthesizing enzyme, DBH (dopamine β-hydroxylase), in comparison with NA receptors-β1, β2, and β3 adrenergic receptors (β1-AR, β2-AR, and β3-AR)-after which we examined the effects of the β-blocker propranolol and α-blockers prazosin and yohimbine on stress-induced microglial activation. Finally, we compared stress-induced microglial activation between wild-type (WT) mice and double-knockout (DKO) mice lacking β1-AR and β2-AR. RESULTS The results demonstrated that (1) microglial activation occurred in most studied brain regions, including the hippocampus (HC), thalamus (TM), and hypothalamus (HT); (2) within these three brain regions, the NA-synthesizing enzyme DBH was densely stained in the neuronal fibers; (3) β1-AR and β2-AR, but not β3-AR, are detected in the whole brain, and β1-AR and β2-AR are co-localized with microglial cells, as observed by laser scanning microscopy; (4) β-blocker treatment inhibited microglial activation in terms of morphology and count through the whole brain; α-blockers did not show such effect; (5) unlike WT mice, DKO mice exhibited substantial inhibition of stress-induced microglial activation in the brain. CONCLUSIONS We demonstrate that neurons/microglia may interact with NA via β1-AR and β2-AR.

中文翻译：

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应激诱导的小胶质细胞激活通过β-肾上腺素受体发生：去甲肾上腺素作为小胶质细胞激活中的关键神经递质。

背景技术已经广泛证明了小胶质细胞参与神经炎症反应。最近的动物研究表明，暴露于急性或慢性应激会诱导大脑中强大的小胶质细胞活化。在本研究中，我们调查了急性应激引起的脑小胶质细胞激活的潜在机制。方法我们首先比较去甲肾上腺素（NA）合成酶DBH（多巴胺β-羟化酶）与NA受体β1，β2和β3肾上腺素能受体（β1-AR，β2-AR和β3-AR）-之后，我们研究了β受体阻断剂普萘洛尔和α受体阻断剂哌唑嗪和育亨宾对应激诱导的小胶质细胞活化的影响。最后，我们比较了野生型（WT）小鼠和缺乏β1-AR和β2-AR的双敲除（DKO）小鼠之间的应激诱导的小胶质细胞活化。结果结果表明：（1）小胶质细胞激活发生在大多数研究的大脑区域，包括海马（HC），丘脑（TM）和下丘脑（HT）；（2）在这三个大脑区域中，NA合成酶DBH在神经元纤维中被密集染色；（3）通过激光扫描显微镜观察，在整个脑中检测到β1-AR和β2-AR，但未检测到β3-AR，并且β1-AR和β2-AR与小胶质细胞共定位。（4）β受体阻滞剂抑制了小胶质细胞的形态和全脑计数。α-受体阻滞剂没有显示出这种作用；（5）与WT小鼠不同，DKO小鼠表现出对应激诱导的大脑小胶质细胞活化的实质抑制作用。结论我们证明神经元/小胶质细胞可能通过β1-AR和β2-AR与NA相互作用。