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大鼠慢性脊髓半切术会导致未受损纤维向运动神经元的传递逐渐下降。

Chronic spinal hemisection in rats induces a progressive decline in transmission in uninjured fibers to motoneurons.

作者信息

Arvanian Victor L, Schnell Lisa, Lou Li, Golshani Roozbeh, Hunanyan Arsen, Ghosh Arko, Pearse Damien D, Robinson John K, Schwab Martin E, Fawcett James W, Mendell Lorne M

机构信息

Department of Neurobiology and Behavior, SUNY at Stony Brook, Life Sciences Building Room 550, Stony Brook, NY 11794-5230, USA.

出版信息

Exp Neurol. 2009 Apr;216(2):471-80. doi: 10.1016/j.expneurol.2009.01.004.

Abstract

Although most spinal cord injuries are anatomically incomplete, only limited functional recovery has been observed in people and rats with partial lesions. To address why surviving fibers cannot mediate more complete recovery, we evaluated the physiological and anatomical status of spared fibers after unilateral hemisection (HX) of thoracic spinal cord in adult rats. We made intracellular and extracellular recordings at L5 (below HX) in response to electrical stimulation of contralateral white matter above (T6) and below (L1) HX. Responses from T6 displayed reduced amplitude, increased latency and elevated stimulus threshold in the fibers across from HX, beginning 1-2 weeks after HX. Ultrastructural analysis revealed demyelination of intact axons contralateral to the HX, with a time course similar to the conduction changes. Behavioral studies indicated partial recovery which arrested when conduction deficits began. In conclusion, this study is the first demonstration of the delayed decline of transmission through surviving axons to individual lumbar motoneurons during chronic stage of incomplete spinal cord injury in adult rats. These findings suggest a chronic pathological state in intact fibers and necessity for prompt treatment to minimize it.

摘要

尽管大多数脊髓损伤在解剖学上是不完全性的,但在人和大鼠的部分损伤模型中,仅观察到有限的功能恢复。为了探究存活纤维为何不能介导更完全的恢复,我们评估了成年大鼠胸段脊髓单侧半横断(HX)后 spared 纤维的生理和解剖状态。我们在 L5(HX 以下)进行细胞内和细胞外记录,以响应 HX 上方(T6)和下方(L1)对侧白质的电刺激。在 HX 后 1 - 2 周开始,来自 T6 的刺激在 HX 对侧的纤维中显示出幅度降低、潜伏期延长和刺激阈值升高。超微结构分析显示 HX 对侧完整轴突的脱髓鞘,其时间进程与传导变化相似。行为学研究表明,当传导缺陷开始时,部分恢复就会停止。总之,本研究首次证明了在成年大鼠不完全性脊髓损伤慢性期,通过存活轴突向单个腰段运动神经元的传导延迟下降。这些发现提示完整纤维存在慢性病理状态,以及需要及时治疗以将其降至最低程度。

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