脊髓损伤后的肌肉源于运动神经元刺激性和突触抑制的变化,而不是突触刺激
Amr Mahrous1, Derin Birch2, C J Heckman1,2
1Departments of Neuroscience.
概括
脊髓损伤 (SCI) 后的肌肉源于抑制受损和运动神经元刺激能力增加,而不是刺激改变. 针对这些机制为SCI恢复提供了更好的治疗潜力.
科学领域:
- 神经科学是一个神经科学.
- 脊髓损伤研究 脊髓损伤研究
- 突触性可塑性 突触性可塑性
背景情况:
- 肌肉是慢性脊髓损伤 (SCI) 的常见并发症,严重影响康复和日常生活.
- 目前治疗的药理疗法通常会抑制刺激输入,从而可能阻碍运动恢复.
研究的目的:
- 调查慢性SCI模型中运动神经元的抑制和刺激突触输入的变化.
- 评估脊髓损伤后运动神经元刺激能力的变化.
- 为了确定更有效的治疗目标来管理SCI后的肌肉.
主要方法:
- 在成年小鼠中诱导完全或不完全的SCI,按功能恢复分类.
- 在体外对神经尾脊髓制剂进行电生理学分析.
- 通过对脊髓根反射的速度依赖性抑制来测量突触抑制.
- 激发性后突触电流 (EPSCs) 和运动神经元中持续的内向电流的评估.
主要成果:
- 慢性SCI制剂表现出类似的活性,但在对照组中没有看到.
- 在慢性SCI模型中发现突触抑制受损.
- 虽然刺激后突触电流保持不变,但在慢性SCI中,运动神经元持续向内的电流增加.
- 药物阻断抑制在所有制剂中诱导了性,在慢性损伤模型中性更长.
结论:
- 慢性SCI中的肌肉主要与减少突触抑制和增加运动神经元刺激性有关.
- 目前针对激发性输入的管理策略可能对运动恢复产生不利影响.
- 恢复突触抑制和调节运动神经元刺激性代表了SCI有前途的治疗途径.
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