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首页> 外文期刊>The European Journal of Neuroscience >Long-term reorganization of respiratory pathways after partial cervical spinal cord injury.
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Long-term reorganization of respiratory pathways after partial cervical spinal cord injury.

机译：颈部分脊髓损伤后呼吸道的长期重组。

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摘要

High cervical spinal cord injury (SCI) interrupts bulbospinal respiratory pathways innervating phrenic motoneurons, and induces an inactivation of phrenic nerves (PN) and diaphragm. We have previously shown that the ipsilateral (ipsi) PN was inactivated following a lateral C2 SCI, but was spontaneously partially reactivated 7 days post-SCI. This phrenic reactivation depended on contralateral (contra) descending pathways, located laterally, that cross the spinal midline. We analysed here whether long-term post-lesional changes may occur in the respiratory network. We showed that ipsi PN reactivation was greater at 3 months compared with 7 days post-SCI, and that it was enhanced after acute contra phrenicotomy (Phx), which also induced a substantial reactivation of the ipsi diaphragm (not detected at 7 days post-SCI). At 3 months post-SCI (compared with 7 days post-SCI), ipsi PN activity was only moderately affected by ipsi Phx or by gallamine treatment, a nicotinic neuromuscular blocking agent, indicating that it was less dependent on ipsi sensory phrenic afferents. After an additional acute contra SCI (C1) performed laterally, ipsi PN activity was abolished in rats 7 days post-SCI, but persisted in rats 3 months post-SCI. This activity thus depended on new functional descending pathways located medially rather than laterally. These may not involve newly recruited neurons as retrograde labelling showed that ipsi phrenic motoneurons were innervated by a similar number of medullary respiratory neurons after a short and long post-lesional time. These results show that after a long post-lesional time, phrenic reactivation is reinforced by an anatomo-functional reorganization of spinal respiratory pathways.
机译：高颈椎脊髓损伤（SCI）中断了pin神经运动神经的支气管脊髓呼吸通路，并导致神经（PN）和diaphragm肌失活。先前我们已经表明，同侧（ipsi）PN在侧向C2 SCI后被灭活，但在SCI后7天被自然地部分激活。这种的激活取决于横穿脊椎中线的对侧（对侧）下降通道。我们在这里分析了呼吸网络中是否可能发生长期的病变后变化。我们发现，与SCI后7天相比，ipsi PN的激活在3个月时更高，并且在急性对侧肾切开术（Phx）后也得到了增强，这也引起了ipsi隔膜的实质性激活（在术后7天未检测到）。 SCI）。 SCI后3个月（SCI后7天），ipsi PN或烟碱神经肌肉阻滞剂没食子胺治疗仅对ipsi PN活性有中等程度的影响，表明它对ipsi感觉传入的依赖性较小。在侧面再次进行急性急性脊髓损伤（C1）后，脊髓损伤后7天大鼠的ipsi PN活性消失，但脊髓损伤后3个月大鼠中ipsi PN活性消失。因此，这种活动取决于位于内侧而不是外侧的新的功能下降途径。这些可能不涉及新近募集的神经元，因为逆行标记​​显示病患经过短时间和长时间后，ipsi运动神经元受类似数量的延髓性呼吸神经元支配。这些结果表明，经过较长的病变后时间，spin的激活通过脊髓呼吸通路的解剖功能重组得到增强。

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