...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neuroscience Methods >A new model of acute compressive spinal cord injury in vitro.
【24h】

A new model of acute compressive spinal cord injury in vitro.

机译：急性急性压迫性脊髓损伤的新模型。

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 novel in vitro method of spinal cord injury was developed to facilitate the study of cellular and molecular mechanisms underlying neural trauma. A 3-cm length of thoracic spinal cord was removed from the adult Wistar rat. A strip of dorsal column and its associated dorsal horn gray matter was excised and pinned in an in vitro recording chamber where it was constantly perfused with oxygenated Ringer's solution at either 25 degrees C or 33 degrees C. Injury was performed by compressing the dorsal column segment in vitro with a modified aneurysm clip (closing force 2.0 g) for 15 s. Microelectrode and sucrose gap recordings were generated to characterize the physiological effects of compressive injury. Longitudinal thin sections of control and injured dorsal column segments were examined by electron microscopy. At 25 degrees C, injured axons were characterized by a significant reduction in amplitude of the compound action potential (CAP) to 76.9 +/- 2.4% (P < 0.0005) and an increase in response latency to 112.5 +/- 2.5% (P <0.005). At 33 degrees C, the effects of injury on the CAP amplitude were accentuated (P< 0.0001). With the K+ channel blocker, 4-AP (1 mM), there was broadening of the CAP of injured axons and a delay in repolarization of the axonal resting membrane potential, suggesting myelin disruption with exposure of paranodal K+ channels. Ultrastructurally, injured dorsal column segments showed considerable axonal and myelin pathology including splaying of the myelin sheath and vesicular degeneration.
机译：开发了一种新的体外脊髓损伤方法，以促进对神经损伤的细胞和分子机制的研究。从成年Wistar大鼠中取出3厘米长的胸脊髓。切下一条背柱带及其相关的背角灰质，并固定在体外记录室中，在该室中在25摄氏度或33摄氏度下不断用含氧林格氏液进行灌注。通过压缩背柱节段进行伤害体外用改良的动脉瘤夹（闭合力2.0 g）持续15 s。产生了微电极和蔗糖间隙记录以表征压迫性损伤的生理效应。对照和受伤的背柱节段的纵向薄切片通过电子显微镜检查。在25摄氏度时，受伤的轴突的特征是复合动作电位（CAP）的幅度显着降低至76.9 +/- 2.4％（P <0.0005），响应潜伏期增加至112.5 +/- 2.5％（P <0.005）。在33摄氏度时，伤害对CAP振幅的影响加剧（P <0.0001）。使用K +通道阻滞剂4-AP（1 mM），受损轴突的CAP变宽，轴突静息膜电位的复极化延迟，这表明髓鞘蛋白因旁淋巴结K +通道暴露而受到破坏。超微结构损伤的背柱节段显示出明显的轴突和髓磷脂病理，包括髓鞘的张开和水泡变性。

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