Central nesfatin-1-expressing neurons are sensitive to peripheral inflammatory stimulus
Central nesfatin-1-expressing neurons are sensitive to peripheral inflammatory stimulus
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DOI：
10.1186/1742-2094-6-27
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发表时间：
2009-09-24
影响因子：
9.3
通讯作者：
Troadec, Jean-Denis
中科院分区：
文献类型：
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作者：
Bonnet, Marion S.;Pecchi, Emilie;Troadec, Jean-Denis
最近，一种新的因子与促肾上腺皮质激素的性质被确定，并称为nesfatin-1。这种蛋白质（82 aac）不仅在外周器官中表达，而且还在位于特定结构的神经元中发现，包括下丘脑和脑干，这两个部位强烈参与食物摄入调节。在这里，我们研究了是否一些神经元，成为激活后的厌食剂量的脂多糖（LPS）注射表现出nesfatin-1表型。为此，我们使用双重免疫组织化学靶向表达的即刻早期基因c-fos和nesfatin-1的冠状冰冻切片的大鼠脑。在报道含有nesfatin-1神经元的免疫敏感结构中评价c-Fos+/nesfatin-1+神经元的数量;即室旁下丘脑核（PVN）、视上核（SON）、弓状核（ARC）和孤束核（NTS）。LPS使PVN、SON和NTS的c-Fos+/nesfatin-1+神经元数量显著增加，ARC的c-Fos +/nesfatin-1+神经元数量增加程度较轻。三重标记表明，一部分的nesfatin-1神经元在NTS内的LPS激活的儿茶酚胺能，因为他们共同表达酪氨酸羟化酶（TH）。因此，我们的数据表明，下丘脑和脑干的nesfatin-1神经元的一部分是敏感的外周炎症信号，并提供了第一个线索表明，中枢释放的nesfatin-1可能有助于导致内毒素性厌食症的神经机制。
Recently, a novel factor with anorexigenic properties was identified and called nesfatin-1. This protein (82 aac) is not only expressed in peripheral organs but it is also found in neurons located in specific structures including the hypothalamus and the brainstem, two sites strongly involved in food intake regulation. Here, we studied whether some of the neurons that become activated following an injection of an anorectic dose of lipopolysaccharides (LPS) exhibit a nesfatin-1 phenotype. To this end, we used double immunohistochemistry to target the expression of the immediate-early gene c-fos and of nesfatin-1 on coronal frozen sections of the rat brain. The number of c-Fos+/nesfatin-1+ neurons was evaluated in the immunosensitive structures reported to contain nesfatin-1 neurons; i.e. paraventricular hypothalamic nucleus (PVN), supraoptic nucleus (SON), arcuate nucleus (ARC) and nucleus of the solitary tract (NTS). LPS strongly increased the number of c-Fos+/nesfatin-1+ neurons in the PVN, SON and NTS, and to a lesser extent in the ARC. Triple labeling showed that a portion of the nesfatin-1 neurons activated in response to LPS within the NTS are catecholaminergic since they co-express tyrosine hydroxylase (TH). Our data therefore indicate that a portion of nesfatin-1 neurons of both the hypothalamus and brainstem are sensitive to peripheral inflammatory signals, and provide the first clues suggesting that centrally released nesfatin-1 may contribute to the neural mechanisms leading to endotoxaemic anorexia.