Sprouting of primary afferent fibers after spinal cord transection in the rat
Sprouting of primary afferent fibers after spinal cord transection in the rat
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DOI：
10.1016/s0306-4522(97)00622-2
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发表时间：
1998-07-01
期刊：
影响因子：
3.3
通讯作者：
Weaver, LC
中科院分区：
文献类型：
--
作者：
Krenz, NR;Weaver, LC
脊髓损伤后，高反射可导致发作性高血压、肌肉痉挛和膀胱协同作用障碍。这种情况可能是由于初级传入纤维的萌发为部分失神经的脊髓中间神经元、自主神经元和运动神经元提供了新的输入。然而，关于脊髓损伤后传入神经突发芽的相互矛盾的报道并没有提供足够的信息来将发芽与高反射联系起来。因此，我们研究了中胸脊髓横断对感觉神经元中央投射的影响，并通过面积测量来量化。脊髓横断后一周，经霍乱毒素B免疫标记的髓鞘传入叶面积在腰椎I-V椎板中较大，但在胸脊髓中没有。小感觉神经元及其无髓鞘纤维的变化，免疫标记的降钙素基因相关肽，评估脊髓和背根神经节。在脐带横断后两周，所有脐带段III-V层降钙素基因相关肽免疫反应纤维的面积增加，但在脐带横断后一周没有增加。对降钙素基因相关肽产生免疫反应的感觉神经元数量没有变化，提示免疫反应面积的增加反映的是发芽，而不是肽的上调。脊髓横断后两周，侧角的免疫反应纤维仅在病变上方和腰椎节段增加。它们与背角纤维不连续，表明它们不是初级传入纤维。使用荧光示踪剂DiI标记传入纤维，在横断后两周，可以看到克拉克核损伤尾侧的面积增加。综上所述，脊髓横断后，有髓鞘和无髓鞘的初级传入纤维，可能还有中间神经元，都发生了部位和时间依赖性的发芽。传入纤维发芽不直接到达自主神经元或运动神经元，但可能通过增加对中间神经元的输入而引起超反射。(c) 1998 ibro。Elsevier Science Ltd.出版。
After spinal cord injury, hyper-reflexia can lead to episodic hypertension, muscle spasticity and urinary bladder dyssynergia. This condition may be caused by primary afferent fiber sprouting providing new input to partially denervated spinal interneurons, autonomic neurons and motor neurons. However, conflicting reports concerning afferent neurite sprouting after cord injury do not provide adequate information to associate sprouting with hyper-reflexia. Therefore, we studied the effect of mid-thoracic spinal cord transection on central projections of sensory neurons, quantified by area measurements. The area of myelinated afferent arbors, immunolabeled by cholera toxin B, was greater in laminae I-V in lumbar, but not thoracic cord, by one week after cord transection. Changes in small sensory neurons and their unmyelinated fibers, immunolabeled for calcitonin gene-related peptide, were assessed in the cord and in dorsal root ganglia. The area of calcitonin gene-related peptide-immunoreactive fibers in laminae III-V increased in all cord segments at two weeks after cord transection, but not at one week. Numbers of sensory neurons immunoreactive for calcitonin gene-related peptide were unchanged, suggesting that the increased area of immunoreactivity reflected sprouting rather than peptide up-regulation. Immunoreactive fibers in the lateral horn increased only above the lesion and in lumbar segments at two weeks after cord transection. They were not continuous with dorsal horn fibers, suggesting that they were not primary afferent fibers. Using the fluorescent tracer DiI to label afferent fibers, an increase in area could be seen in Clarke's nucleus caudal to the injury two weeks after transection.In conclusion, site-and time-dependent sprouting of myelinated and unmyelinated primary afferent fibers, and possibly interneurons, occurred after spinal cord transection. Afferent fiber sprouting did not reach autonomic or motor neurons directly, but may cause hyper-reflexia by increasing inputs to interneurons. (C) 1998 IBRO. Published by Elsevier Science Ltd.