• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Brain research >The reaction of cerebral cortex to a nearby lesion: Damage, survival, self-protection
【24h】

The reaction of cerebral cortex to a nearby lesion: Damage, survival, self-protection

机译：大脑皮层对附近病变的反应：损害，生存，自我保护

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

A needlestick injury to cerebral cortex causes immediate damage along the track of the needle (haemorrhage, cell death) and sequelae (the formation of amyloid-positive plaques, extracellular deposits of hyperphosphorylated tau protein, microglial proliferation, astrogliosis) that are long lasting, and mimic the neuropathology associated with Alzheimer's disease. We report here that the same injury also elicits a distinctive response in the cortex flanking (up to 1 mm from) the direct injury. Needlestick injury was made in the neo- and hippocampal cortex of young (3 months) healthy Sprague-Dawley rats. After survival times of up to 7 d, the response of the cortex was assessed with histology, immunohistochemistry and stereology. Uptake of FluoroJade B at 1 d survival and labelling for 4-hydroxynonenal (4-HNE) gave measures of membrane damage; labelling for 8-hydroxy-2'-deoxyguanosine (8-OHDG) gave a measure of DNA damage, and labelling with the AT8 antibody gave a measure of the hyperphosphorylation of tau. Two probes, for neuroglobin and basic fibroblast growth factor (FGF-2), gave measures of a self-protective response in the tissue. Results indicate that neurones in the flanking region are damaged by the nearby lesion, and within 1 d upregulate self-protective mechanisms. Over the next 6 d survival, evidence of neuronal damage reduces markedly. In summary, cells in the region flanking a lesion are stressed by the lesion, and react to the stress with a self-protective response, which prevents their death. This response may be an important, previously unrecognised feature of brain tissue close to a focus of stress, such as a microhaemorrhage. (C) 2015 Elsevier B.V. All rights reserved.
机译：大脑皮层的针刺伤会导致长期持续的沿针迹的损伤（出血，细胞死亡）和后遗症（淀粉样蛋白阳性斑块，高磷酸化tau蛋白的细胞外沉积，小胶质细胞增生，星形胶质变）。模拟与阿尔茨海默氏病相关的神经病理学。我们在这里报告说，相同的损伤也引起直接损伤侧翼（距最大1毫米）的皮层有独特的反应。幼鼠（3个月）健康的Sprague-Dawley大鼠的新皮层和海马皮层造成了针刺损伤。存活时间长达7 d后，通过组织学，免疫组织化学和立体学评估皮质的反应。存活1d时摄取FluoroJade B，并标记4-羟基壬烯醛（4-HNE）可以测量膜损伤。标记8-羟基-2'-脱氧鸟苷（8-OHDG）可以测量DNA损伤，而用AT8抗体标记可以测量tau的过度磷酸化。两种针对神经球蛋白和碱性成纤维细胞生长因子（FGF-2）的探针可测量组织中的自我保护反应。结果表明，侧翼区域的神经元受到附近病变的损害，并在1 d内上调自我保护机制。在接下来的6天生存期中，神经元损伤的证据明显减少。总之，位于病变侧翼的区域中的细胞受到病变的压力，并通过自我保护反应对应激作出反应，从而防止其死亡。这种反应可能是接近压力焦点（例如微出血）的脑组织的重要的，以前无法识别的特征。 （C）2015 Elsevier B.V.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号