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首页> 外文期刊>The European Journal of Neuroscience >Alteration of the cell adhesion molecule L1 expression in a specific subset of primary afferent neurons contributes to neuropathic pain.
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Alteration of the cell adhesion molecule L1 expression in a specific subset of primary afferent neurons contributes to neuropathic pain.

机译：在原发传入神经元的特定子集中细胞粘附分子L1表达的改变有助于神经性疼痛。

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摘要

The cell adhesion molecule L1 (L1-CAM) plays important functional roles in the developing and adult nervous systems. Here we show that peripheral nerve injury induced dynamic post-transcriptional alteration of L1-CAM in the rat dorsal root ganglia (DRGs) and spinal cord. Sciatic nerve transection (SCNT) changed the expression of L1-CAM protein but not L1-CAM mRNA. In DRGs, SCNT induced accumulation of the L1-CAM into the surface of somata, which resulted in the formation of immunoreactive ring structures in a number of unmyelinated C-fiber neurons. These neurons with L1-CAM-immunoreactive ring structures were heavily colocalized with phosphorylated p38 MAPK. Western blot analysis revealed the increase of full-length L1-CAM and decrease of fragments of L1-CAM after SCNT in DRGs. Following SCNT, L1-CAM-immunoreactive profiles in the dorsal horn showed an increase mainly in pre-synaptic areas of laminae I-II with a delayed onset and colocalized with growth-associated protein 43. In contrast to DRGs, SCNT increased the proteolytic 80-kDa fragment of L1-CAM and decreased full-length L1-CAM in the spinal cord. The intrathecal injection of L1-CAM antibody for the extracellular domain of L1-CAM inhibited activation of p38 MAPK and emergence of ring structures of L1-CAM immunoreactivity in injured DRG neurons. Moreover, inhibition of extracellular L1-CAM binding by intrathecal administration of antibody suppressed the mechanical allodynia and thermal hyperalgesia induced by partial SCNT. Collectively, these data suggest that the modification of L1-CAM in nociceptive pathways might be an important pathomechanism of neuropathic pain.
机译：细胞粘附分子L1（L1-CAM）在发育中的和成年的神经系统中起着重要的功能作用。在这里，我们显示，周围神经损伤在大鼠背根神经节（DRGs）和脊髓中诱导了L1-CAM的动态转录后改变。坐骨神经横切（SCNT）改变L1-CAM蛋白的表达，但不改变L1-CAM mRNA的表达。在DRG中，SCNT诱导L1-CAM积累到躯体表面，这导致在许多未髓鞘的C纤维神经元中形成免疫反应性环结构。这些具有L1-CAM免疫反应性环状结构的神经元与磷酸化的p38 MAPK紧密共定位。 Western blot分析显示DRGs中SCNT后全长L1-CAM增加而L1-CAM片段减少。继SCNT之后，背角的L1-CAM免疫反应谱显示主要在层状I-II的突触前区域增加，具有延迟发作并与生长相关蛋白43共定位。与DRG相比，SCNT增加了蛋白水解80 L1-CAM的-kDa片段和脊髓中全长L1-CAM减少。鞘内注射L1-CAM抗体对L1-CAM的胞外域抑制了受损DRG神经元中p38 MAPK的激活和L1-CAM免疫反应性环结构的出现。此外，鞘内施用抗体抑制细胞外L1-CAM结合可抑制部分SCNT引起的机械异常性疼痛和热痛觉过敏。总的来说，这些数据表明在伤害感受途径中L1-CAM的修饰可能是神经性疼痛的重要发病机制。

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