Restoration of contralateral representation in the mouse somatosensory cortex after crossing nerve transfer.

Restoration of contralateral representation in the mouse somatosensory cortex after crossing nerve transfer.
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DOI:
10.1371/journal.pone.0035676
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Shibuki K
Shibuki K
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Yamashita H;Chen S;Komagata S;Hishida R;Iwasato T;Itohara S;Yagi T;Endo N;Shibata M;Shibuki K

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臂丛神经 (BP) 中脊神经根的撕脱可以通过神经移植物的交叉神经转移将受伤的神经末端连接到病变侧对侧的 BP 来修复。这些患者的感觉恢复表明对侧初级体感皮层 (S1) 被绕过对侧 BP 的传入输入激活。为了证实这一假设,本研究通过使用经颅黄素蛋白荧光成像对小鼠跨神经转移后的皮质活动进行可视化。在幼稚小鼠中,施加于前爪的振动刺激会在受刺激侧对侧的 S1 中引起局部荧光反应,而同侧 S1 中几乎没有活动。交叉神经转移后 4 周,受伤侧和修复侧的前爪刺激仅导致受刺激侧同侧的 S1 皮质反应。交叉神经转移后八周,前爪刺激导致两个半球的 S1 皮质反应。通过切断用于修复的神经移植物,可以消除这些皮质反应。将同侧 S1 暴露于蓝色激光会抑制同侧 S1 以及对侧 S1 的皮质反应,表明同侧反应通过皮质-皮质通路传播到对侧 S1。直接高频刺激同侧 S1 与前爪刺激相结合,可急性诱导幼鼠前爪区域的 S1 双侧皮质表征。在皮质限制性异型 GluN1 (NMDAR1) 敲除小鼠中,交叉神经转移后对侧 S1 的皮质反应减少。在两个半球 S1 之间的皮质-皮质通路受损的基因操纵小鼠中,没有清楚地观察到功能性双侧皮质表征。总而言之,这些发现强烈表明,皮质-皮质通路的活动依赖性增强对于跨神经转移后患者的感觉恢复具有关键作用。
Avulsion of spinal nerve roots in the brachial plexus (BP) can be repaired by crossing nerve transfer via a nerve graft to connect injured nerve ends to the BP contralateral to the lesioned side. Sensory recovery in these patients suggests that the contralateral primary somatosensory cortex (S1) is activated by afferent inputs that bypassed to the contralateral BP. To confirm this hypothesis, the present study visualized cortical activity after crossing nerve transfer in mice through the use of transcranial flavoprotein fluorescence imaging. In naïve mice, vibratory stimuli applied to the forepaw elicited localized fluorescence responses in the S1 contralateral to the stimulated side, with almost no activity in the ipsilateral S1. Four weeks after crossing nerve transfer, forepaw stimulation in the injured and repaired side resulted in cortical responses only in the S1 ipsilateral to the stimulated side. At eight weeks after crossing nerve transfer, forepaw stimulation resulted in S1 cortical responses of both hemispheres. These cortical responses were abolished by cutting the nerve graft used for repair. Exposure of the ipsilateral S1 to blue laser light suppressed cortical responses in the ipsilateral S1, as well as in the contralateral S1, suggesting that ipsilateral responses propagated to the contralateral S1 via cortico-cortical pathways. Direct high-frequency stimulation of the ipsilateral S1 in combination with forepaw stimulation acutely induced S1 bilateral cortical representation of the forepaw area in naïve mice. Cortical responses in the contralateral S1 after crossing nerve transfer were reduced in cortex-restricted heterotypic GluN1 (NMDAR1) knockout mice. Functional bilateral cortical representation was not clearly observed in genetically manipulated mice with impaired cortico-cortical pathways between S1 of both hemispheres. Taken together, these findings strongly suggest that activity-dependent potentiation of cortico-cortical pathways has a critical role for sensory recovery in patients after crossing nerve transfer.
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