...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell and Tissue Research >Viral interference with neuronal integrity: what can we learn from the Borna disease virus?
【24h】

Viral interference with neuronal integrity: what can we learn from the Borna disease virus?

机译：病毒对神经元完整性的干扰：我们可以从博尔纳病病毒中学到什么？

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

The neurotropic Borna disease virus (BDV) is unusual in that it can persistently infect neurons of the central nervous system (CNS) without causing general cell death, reflecting its favourable adaptation to the brain. The activity-dependent enhancement of neuronal network activity is however disturbed after BDV infection, possibly by its effect on the protein kinase C signalling pathway. The best model for studying BDV, which has a non-cytolytic replication strategy in primary neurons, is the rat. Infection of adult rats results in a fatal immune-mediated disease, whereas BDV establishes persistent infection of the brain in newborn rats resulting in progressive neuronal cell loss in defined regions of the CNS. Our recently developed system of BDV-infected hippocampal slice cultures has clearly shown that the onset of granule cell loss begins after the formation of the mossy fibre projection. Quantitative analysis has revealed a significant increase in synaptic density on identified remaining granule cell dendrites at 6 weeks after infection, followed by a decline. Granule cells are the major target of entorhinal afferents. However, despite an almost complete loss of dentate granule cells during BDV infection, entorhinal axons persist in their correct layer, both in vivo and in slice cultures, possibly exploiting rewiring capabilities and thereby allowing new synapse formation with available targets. These morphological observations, together with electrophysiological and biochemical data, indicate that BDV is a suitable model virus for studying virus-induced morphological and functional changes of neurons and connectivity patterns.
机译：嗜神经性博尔纳病病毒（BDV）之所以与众不同，是因为它可以持续感染中枢神经系统（CNS）的神经元而不会引起一般细胞死亡，这反映了它对大脑的良好适应性。然而，BDV感染后，神经元网络活动的活动依赖性增强受到干扰，这可能是由于其对蛋白激酶C信号通路的影响。在原代神经元中具有非细胞溶解复制策略的BDV研究的最佳模型是大鼠。成年大鼠的感染导致致命的免疫介导的疾病，而BDV在新生大鼠中建立了大脑的持续感染，导致CNS定义区域的神经元细胞逐渐丢失。我们最近开发的BDV感染的海马切片培养物系统清楚地表明，在长满苔藓的纤维突起后开始出现颗粒细胞损失。定量分析显示，感染后6周，识别出的剩余颗粒细胞树突的突触密度显着增加，然后下降。颗粒细胞是内啡肽传入的主要靶标。然而，尽管在BDV感染过程中齿状颗粒细胞几乎完全丧失，但内嗅轴突仍在体内和切片培养物中均保留在其正确的层中，可能利用了重新接线的能力，从而允许与可用靶标形成新的突触。这些形态学观察以及电生理和生化数据表明，BDV是研究病毒诱导的神经元形态和功能变化以及连通性模式的合适模型病毒。

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