Mild-traumatic brain injury (mTBI) represents ~80% of all emergency room visits and increases the probability of developing long-term cognitive disorders in children. To date, molecular and cellular mechanisms underlying post-mTBI cognitive dysfunction are unknown. Astrogliosis has been shown to significantly alter astrocytes' properties following brain injury, potentially leading to significant brain dysfunction. However, such alterations have never been investigated in the context of juvenile mTBI (jmTBI). A closed-head injury model was used to study jmTBI on postnatal-day 17 mice. Astrogliosis was evaluated using glial fibrillary acidic protein (GFAP), vimentin, and nestin immunolabeling in somatosensory cortex (SSC), dentate gyrus (DG), amygdala (AMY), and infralimbic area (ILA) of prefrontal cortex in both hemispheres from 1 to 30 days postinjury (dpi). In vivo T2-weighted-imaging (T2WI) and diffusion tensor imaging (DTI) were performed at 7 and 30 dpi to examine tissue level structural alterations. Increased GFAP-labeling was observed up to 30 dpi in the ipsilateral SSC, the initial site of the impact. However, vimentin and nestin expression was not perturbed by jmTBI. The morphology of GFAP positive cells was significantly altered in the SSC, DG, AMY, and ILA up to 7 dpi that some correlated with magnetic resonance imaging changes. T2WI and DTI values were significantly altered at 30 dpi within these brain regions most prominently in regions distant from the impact site. Our data show that jmTBI triggers changes in astrocytic phenotype with a distinct spatiotemporal pattern. We speculate that the presence and time course of astrogliosis may contribute to pathophysiological processes and long-term structural alterations following jmTBI.

中文翻译：

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少年轻度脑外伤会引起不同的时空星形胶质细胞反应。

轻度创伤性脑损伤（mTBI）占所有急诊室就诊的80％，并增加了儿童患长期认知障碍的可能性。迄今为止，尚不清楚mTBI后认知功能障碍的分子和细胞机制。星形胶质沉着症已被证明会在脑损伤后显着改变星形胶质细胞的特性，并可能导致严重的脑功能障碍。但是，从未在少年mTBI（jmTBI）的背景下研究过这种改变。闭颅损伤模型用于研究出生后第17天的小鼠的jmTBI。使用胶质纤维酸性蛋白（GFAP），波形蛋白和Nestin免疫标记在体感皮层（SSC），齿状回（DG），杏仁核（AMY），损伤后1到30天（dpi），两个半球的前额叶皮质下缘面积（ILA）。以7和30 dpi进行体内T2加权成像（T2WI）和扩散张量成像（DTI），以检查组织水平的结构改变。在同侧SSC（影响的最初部位）中，观察到高达30 dpi的GFAP标记增加。但是，波形蛋白和巢蛋白的表达不受jmTBI的干扰。高达7 dpi的SSC，DG，AMY和ILA中GFAP阳性细胞的形态发生了显着变化，其中一些与磁共振成像的变化有关。在这些脑区域中，距撞击点较远的区域中，最明显的是T2WI和DTI值在30 dpi时发生了显着变化。我们的数据表明，jmTBI以独特的时空模式触发星形细胞表型的变化。