Experimental epidural hematoma causes cerebral infarction and activates neocortical glial and neuronal genesis in adult guinea pigs
Experimental epidural hematoma causes cerebral infarction and activates neocortical glial and neuronal genesis in adult guinea pigs
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DOI：
10.1002/jnr.23148
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发表时间：
2013-02
影响因子：
4.2
通讯作者：
A. Pan;Ming Li;Junli Gao;Zhi‐Qin Xue;Zhiyuan Li;Xian-Yui Yuan;Duan-Wu Luo;Xue-gang Luo;
中科院分区：
文献类型：
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作者：
A. Pan;Ming Li;Junli Gao;Zhi‐Qin Xue;Zhiyuan Li;Xian-Yui Yuan;Duan-Wu Luo;Xue-gang Luo;
硬膜外血肿（EDH）是一种危及生命的创伤性脑损伤。关于EDH可能在多大程度上引起大脑皮层的神经损伤和再生反应知之甚少。在这里，我们试图通过使用豚鼠作为实验模型来探索这些问题。通过向硬膜外腔注射0.1 ml自体血诱导单侧EDH，在损伤后7、14、30和60天检查实验效果。损伤后7天，在EDH深部的皮质中发生梗死，中央梗死区域I至V层发生神经元死亡，神经元特异性核抗原（NeuN）的免疫反应性（IR）丧失证明了这一点。胶质细胞酸性蛋白（GFAP）免疫反应呈细胞带，环绕梗死灶，沿软脑膜沿着向梗死周围皮质延伸。双皮质素（DCX）IR出现在这些相同的领域，与标记的细胞出现星形胶质细胞和神经元的配置文件。DCX/GFAP共定位通常在损伤后7天和14天在这些区域发现，而DCX/NeuN共标记的神经元在损伤后30天和60天可检测到。与内源性增殖标记物Ki-67或溴脱氧尿苷（BrdU）进行脉冲追踪后，GFAP-、DCX-或NeuN-免疫反应性细胞亚群与该标记物共定位。结果表明，实验性EDH可引起严重的神经元丢失，诱导明显的胶质细胞活化，并促进一定程度的局部神经元的发生。这些发现指出了在EDH的临床管理中改善神经元恢复的潜在治疗靶点。© 2012 Wiley Periodicals，Inc.
Epidural hematoma (EDH) is a type of life‐threatening traumatic brain injury. Little is known about the extent to which EDH may cause neural damage and regenerative response in the cerebral cortex. Here we attempted to explore these issues by using guinea pigs as an experimental model. Unilateral EDH was induced by injection of 0.1 ml autologous blood into the extradural space, with experimental effects examined at 7, 14, 30, and 60 days postlesion. An infarct developed in the cortex deep to the EDH largely after 7 days postlesion, with neuronal death occurred from layers I to V in the central infarct region, as evidenced by loss of immunoreactivity (IR) for neuron‐specific nuclear antigen (NeuN). Glial fibrillary acidic protein (GFAP) IR appeared as a cellular band surrounding the infarct and extending into the periinfarct cortex along the pia. Doublecortin (DCX) IR emerged in these same areas, with labeled cells appearing as astrocytic and neuronal profiles. DCX/GFAP colocalization was found in these regions commonly at 7 and 14 days postlesion, whereas DCX/NeuN‐colabeled neurons were detectable at 30 and 60 days postlesion. Subpopulations of GFAP‐, DCX‐, or NeuN‐immunoreactive cells colocalized with the endogenous proliferative marker Ki‐67 or bromodeoxyuridine (BrdU) after pulse‐chase with this birth‐dating marker. The results suggest that experimental EDH can cause severe neuronal loss, induce significant glial activation, and promote a certain degree of local neuronal genesis in adult guinea pig neocortex. These findings point to potential therapeutic targets for improving neuronal recovery in clinical management of EDH. © 2012 Wiley Periodicals, Inc.