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首页> 美国卫生研究院文献>eNeuro >Afferent Fiber Remodeling in the Somatosensory Thalamus of Mice as a Neural Basis of Somatotopic Reorganization in the Brain and Ectopic Mechanical Hypersensitivity after Peripheral Sensory Nerve Injury
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Afferent Fiber Remodeling in the Somatosensory Thalamus of Mice as a Neural Basis of Somatotopic Reorganization in the Brain and Ectopic Mechanical Hypersensitivity after Peripheral Sensory Nerve Injury

机译：小鼠体感性丘脑的传入纤维重塑作为大脑中体位重组和周围感觉神经损伤后异位机械性超敏反应的神经基础

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Plastic changes in the CNS in response to peripheral sensory nerve injury are a series of complex processes, ranging from local circuit remodeling to somatotopic reorganization. However, the link between circuit remodeling and somatotopic reorganization remains unclear. We have previously reported that transection of the primary whisker sensory nerve causes the abnormal rewiring of lemniscal fibers (sensory afferents) on a neuron in the mouse whisker sensory thalamus (V2 VPM). In the present study, using transgenic mice whose lemniscal fibers originate from the whisker sensory principle trigeminal nucleus (PrV2) are specifically labeled, we identified that the transection induced retraction of PrV2-originating lemniscal fibers and invasion of those not originating from PrV2 in the V2 VPM. This anatomical remodeling with somatotopic reorganization was highly correlated with the rewiring of lemniscal fibers. Origins of the non-PrV2-origin lemniscal fibers in the V2 VPM included the mandibular subregion of trigeminal nuclei and the dorsal column nuclei (DCNs), which normally represent body parts other than whiskers. The transection also resulted in ectopic receptive fields of V2 VPM neurons and extraterritorial pain behavior on the uninjured mandibular region of the face. The anatomical remodeling, emergence of ectopic receptive fields, and extraterritorial pain behavior all concomitantly developed within a week and lasted more than three months after the transection. Our findings, thus, indicate a strong linkage between these plastic changes after peripheral sensory nerve injury, which may provide a neural circuit basis underlying large-scale reorganization of somatotopic representation and abnormal ectopic sensations.
机译：响应于周围感觉神经损伤的CNS塑性变化是一系列复杂的过程，从局部回路重塑到体位重组。但是，电路重塑和体位重组之间的联系仍然不清楚。我们以前曾报道过，原须的感觉神经横断会导致老鼠须感觉丘脑（V2 VPM）的神经元上神经元纤维（感觉传入）的异常重新布线。在本研究中，使用标记了睑缘纤维源自晶须感觉原理三叉神经核（PrV2）的转基因小鼠，我们确定了横断面诱导了PrV2起源的睑缘纤维的回缩以及非源自PrV2的那些在V2中的侵袭。 VPM。具有体位重组的这种解剖重塑与双侧睑缘纤维的重排高度相关。 V2 VPM中非Prv2来源的次生鳞茎纤维的起源包括三叉神经核的下颌子区域和背柱核（DCN），它们通常代表除须晶之外的身体部位。横切还导致V2 VPM神经元的异位接受域和面部未受伤的下颌区域的域外疼痛行为。解剖重建，异位感受野的出现以及域外疼痛行为均在一周内发生，并在横断后持续三个多月。因此，我们的发现表明周围感觉神经损伤后这些可塑性变化之间有很强的联系，这可能为躯体表位代表和异常异位感觉的大规模重组提供了神经回路基础。

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