Evolution of post-traumatic neurodegeneration after controlled cortical impact traumatic brain injury in mice and rats as assessed by the de Olmos silver and fluorojade staining methods

Evolution of post-traumatic neurodegeneration after controlled cortical impact traumatic brain injury in mice and rats as assessed by the de Olmos silver and fluorojade staining methods
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DOI:
10.1089/neu.2007.0383
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发表时间:
2008-03-01
影响因子:
4.2
通讯作者:
Sullivan, Patrick G.
Sullivan, Patrick G.
中科院分区:
医学2区
文献类型:
--
作者:
Hall, Edward D.;Bryant, Ying Deng;Sullivan, Patrick G.

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本报告记录了使用de Olmos氨基铜银染色法对小鼠和大鼠受控皮质撞击(CCI)创伤性脑损伤(TBI)后前7天内创伤后神经变性的分析,该方法选择性染色变性轴突和神经末梢,而fluorojade方法染色变性神经元细胞体。在这两个物种中,在损伤后的第一个48小时内观察到皮质、海马和丘脑变性的进行性增加。在48 h时,约50%的同侧皮质体积被染色。同样,背侧海马在所有子区域中显示出广泛的变性。这包括CA 1、CA 3、CA 4和fluorojade显示的齿状细胞体,以及通过银染色鉴定的传入和传出海马投射区域的高度轴突变性。这些结果表明,以前的CCI研究,依赖于传统的组织学方法,显示细胞体染色单独低估了与CCI-TBI模型相关的轴突损伤的程度。为了捕捉轴突和细胞体损伤的全部程度,分别需要结合银染色和fluorojade染色。潜在的神经保护剂的未来研究可能不应该依赖于皮质病变体积或体积的测量备用皮质组织单独使用传统的组织学染色,因为这些不能确定创伤后神经病理学的完整程度,一些代理商,减少皮质病变体积可能无法影响。
This report documents an analysis of post-traumatic neurodegeneration during the first 7 days after controlled cortical impact ( CCI) traumatic brain injury ( TBI) in mice and rats using the de Olmos aminocupric silver staining method, which selectively stains degenerating axons and nerve terminals, compared to the fluorojade method, which stains degenerating neuronal cell bodies. A progressive increase in cortical, hippocampal, and thalamic degeneration was observed over the first 48 h after injury in both species. Approximately 50% of the ipsilateral cortical volume was stained at 48 h. Similarly, the dorsal hippocampus showed widespread degeneration in all of the subfields. This included CA1, CA3, CA4, and dentate cell bodies revealed by fluorojade together with a high degree of axonal degeneration in areas carrying afferent and efferent hippocampal projections that is identified by silver staining. These results show that previous CCI studies which have relied on conventional histological methods that show cell body staining alone have underestimated the degree of axonal damage associated with the CCI-TBI model. In order to capture the full extent of the injury to both axons and cell bodies, the combination of silver staining and fluorojade staining is needed, respectively. Future studies of potential neuroprotective agents should probably not rely on the measure of cortical lesion volume or volume of spared cortical tissue using conventional histological stains alone, since these fail to identify the complete extent of the posttraumatic neuropathology that some agents which reduce cortical lesion volume may not be able to effect.