在受伤的脊髓中通过KCC2操纵重新激活休眠的继电路
1F.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Cell
|July 24, 2018
概括
通过增强休眠中继电路,KCC2激动剂恢复了脊髓损伤的小鼠的步行能力. 这表明KCC2激动剂有望促进脊髓损伤后的功能恢复.
科学领域:
- 神经科学
- 脊髓损伤研究
- 分子医学
背景情况:
- 许多脊髓损伤是不完整的, 但导致完全.
- 不知道为什么被遗留的轴突无法恢复功能.
- 在受伤后的腰椎中存在休眠的继电路.
研究的目的:
- 调查为什么幸存的轴突无法在脊髓损伤后进行功能恢复.
- 确定促进功能恢复的治疗目标.
主要方法:
- 在小鼠中进行小分子查,两侧半截切.
- 通过恢复步行能力评估功能恢复.
- 研究了KCC2和抑制性内神经元的作用.
主要成果:
- 一种KCC2激动剂恢复了小鼠的步行能力.
- 在抑制性内神经元中选择性KCC2表达或超极化DREADD模仿了这种效应.
- 治疗将功能障碍的脊柱回路转化为功能状态, 促进下降输入中继.
结论:
- 脊柱抑制性内部神经元作为一个阻碍下降输入损伤后的整合.
- 在脊髓损伤后,KCC2激动剂有望促进功能恢复.
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