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首页> 外文期刊>The European Journal of Neuroscience >Peripheral nerve injury induces reorganization of galanin-containing afferents in the superficial dorsal horn of monkey spinal cord.
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Peripheral nerve injury induces reorganization of galanin-containing afferents in the superficial dorsal horn of monkey spinal cord.

机译：周围神经损伤导致猴子脊髓浅背角的含甘丙肽的传入受体重组。

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摘要

Peripheral nerve injury-induced structural and chemical modifications of the sensory circuits in the dorsal horn of the spinal cord contribute to the mechanism of neuropathic pain. In contrast to the topographic projection of primary afferents in laminae I-IV in the rat spinal cord, the primary afferents of Macaca mulatta monkeys almost exclusively project into laminae I-II of the spinal cord. After peripheral nerve injury, up-regulation of galanin has been found in sensory neurons in both monkey and rat dorsal root ganglia. However, the nerve injury-induced ultrastructural modification of galanin-containing afferents in the monkey spinal cord remains unknown. Using immunoelectron microscopy, we found that 3 weeks after unilateral sciatic nerve transection, the number of galanin-containing afferents was increased in ipsilateral lamina II of monkey spinal cord. Branching of these galanin-positive afferents was often observed. The afferent terminals contained a large number of synaptic vesicles, peptidergic vesicles and mitochondria, whereas the number of synapses was markedly reduced. Some of the afferents-enriched microtubules were often packed into bundles. Moreover, galanin-labeling could be associated with endosomal structures in many dendrites and axonal terminals of dorsal horn neurons. These results suggest that peripheral nerve injury induces an expansion of the central projection of galanin-containing afferents in lamina II of the monkey spinal cord, not only by increasing galanin levels in primary afferents but also by triggering afferent branching.
机译：周围神经损伤引起的脊髓背角感觉回路的结构和化学修饰有助于神经性疼痛的机制。与大鼠脊髓中层I-IV的主要传入体的地形图投影相反，猕猴的主要传入体几乎完全伸入脊髓的层I-II。周围神经损伤后，在猴和大鼠背根神经节的感觉神经元中都发现了甘丙肽的上调。然而，神经损伤引起的猴子脊髓中含有甘丙肽的传入神经的超微结构修饰仍然未知。使用免疫电子显微镜，我们发现单侧坐骨神经横断3周后，猴脊髓同侧椎板II中含甘丙肽的传入神经数目增加。经常观察到这些甘丙肽阳性传入分支。传入端包含大量的突触小泡，肽能小泡和线粒体，而突触的数量明显减少。一些富含传入微管的微管通常被打包成束。此外，甘丙肽标记可能与背角神经元的许多树突和轴突末端的内体结构有关。这些结果表明，外周神经损伤不仅通过增加初级传入神经中的丙氨酸水平，而且还通过触发传入分支来诱导猴脊髓椎板II内含甘丙肽的传入神经的中心投射的扩展。

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