Cortical stimulation leads to shortened myelin sheaths and increased axonal branching in spared axons after cervical spinal cord injury.
Cortical stimulation leads to shortened myelin sheaths and increased axonal branching in spared axons after cervical spinal cord injury.
复制标题
颈髓损伤后，皮质刺激导致髓鞘缩短，幸存轴突的轴突分支增加。
作者：
Kondiles,BR;Murphy,RL;Widman,AJ;Perlmutter,SI;Horner,PJ
神经活动和学习导致完整中枢神经系统（CNS）中髓鞘的可塑性，但CNS损伤后这种可塑性尚未得到充分研究。在脊髓损伤（SCI）的情况下，脱髓鞘发生在病变部位，存活轴突的自然髓鞘再生可能需要数月。为了确定神经活动是否调节损伤的成年CNS中的髓鞘和轴突可塑性，我们以10 Hz电刺激损伤对侧运动皮层，以驱动亚慢性脊髓挫伤大鼠皮质脊髓束中的神经活动。我们量化髓鞘和轴突的特点，通过追踪皮质脊髓轴突吻侧和病变震中，并确定节点的Ranvier免疫组织化学。三周的日常刺激诱导非常短的髓鞘，轴突分支，和更薄的轴突外的病变区，重塑以前没有报道。令人惊讶的是，重塑在损伤的嘴侧特别强烈，这表明电刺激可以促进白色物质的可塑性，即使在没有被挫伤直接脱髓鞘的区域。刺激没有改变损伤部位的髓鞘或轴突，这表明在亚慢性期，神经元活动不会导致损伤附近的髓鞘重塑。这些数据首次证明了成熟的长束运动通路的结和髓鞘结构对电刺激的反应的大规模重塑。这一发现表明，神经调节促进损伤后通路完整区域的白色物质可塑性，并提出了关于轴突和髓鞘可塑性之间相互作用的有趣问题。
Neural activity and learning lead to myelin sheath plasticity in the intact central nervous system (CNS), but this plasticity has not been well‐studied after CNS injury. In the context of spinal cord injury (SCI), demyelination occurs at the lesion site and natural remyelination of surviving axons can take months. To determine if neural activity modulates myelin and axon plasticity in the injured, adult CNS, we electrically stimulated the contralesional motor cortex at 10 Hz to drive neural activity in the corticospinal tract of rats with sub‐chronic spinal contusion injuries. We quantified myelin and axonal characteristics by tracing corticospinal axons rostral to and at the lesion epicenter and identifying nodes of Ranvier by immunohistochemistry. Three weeks of daily stimulation induced very short myelin sheaths, axon branching, and thinner axons outside of the lesion zone, where remodeling has not previously been reported. Surprisingly, remodeling was particularly robust rostral to the injury which suggests that electrical stimulation can promote white matter plasticity even in areas not directly demyelinated by the contusion. Stimulation did not alter myelin or axons at the lesion site, which suggests that neuronal activity does not contribute to myelin remodeling near the injury in the sub‐chronic period. These data are the first to demonstrate wide‐scale remodeling of nodal and myelin structures of a mature, long‐tract motor pathway in response to electrical stimulation. This finding suggests that neuromodulation promotes white matter plasticity in intact regions of pathways after injury and raises intriguing questions regarding the interplay between axonal and myelin plasticity.