Acute and chronic changes in dorsal horn innervation by primary afferents and descending supraspinal pathways after spinal cord injury
Acute and chronic changes in dorsal horn innervation by primary afferents and descending supraspinal pathways after spinal cord injury
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DOI：
10.1002/cne.21412
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发表时间：
2007-09-02
影响因子：
2.5
通讯作者：
Keast, Janet R.
中科院分区：
文献类型：
--
作者：
Kalous, Adrianna;Osborne, Peregrine B.;Keast, Janet R.
脊髓损伤（SCI）后，肽能伤害性感受的萌发和脊髓上向背角的下降投射被认为是神经性疼痛的机制。为了确定可能引发或维持 SCI 疼痛的结构变化，我们使用大鼠的完整横断模型来检查病变处背角喙部的结构重塑与损伤距离、层流区域和损伤持续时间的关系。主要类别的 C 纤维初级传入神经对结构和化学变化的敏感性以及承受可塑性的能力差异很大。肽能初级传入神经在靠近损伤部位的背角节段中显示出广泛的损失。这种损失部分可能是由于神经肽表达减少所致。肽能纤维的减少是暂时的，表明代偿性发芽，并且可能还增加了脊髓内神经肽的表达。表达 GFR α 1 的非肽能传入神经很大程度上不受 SCI 的影响。相反，在表达 GFR α 2 的非肽能传入神经中，SCI 导致背角神经支配的永久性丧失。出乎意料的是，GFR α 2 在整个更深的椎板中被短暂诱导，但这并不是由于背根神经节中 GFR α 2 的上调。我们还观察到脊髓上起源的儿茶酚胺末端永久发芽。这仅限于浅层。我们的结果表明，SCI 导致感觉输入丧失以及结构重塑，从而导致伤害性输入和下行调制的平衡被永久改变。这些变化可能有助于 SCI 部位的喙部机制触发和维持神经性疼痛。
Sprouting of peptidergic nociceptive and descending supraspinal projections to the dorsal horn following spinal cord injury (SCI) has been proposed as a mechanism of neuropathic pain. To identify structural changes that could initiate or maintain SCI pain, we used a complete transection model in rats to examine how structural remodeling in the dorsal horn rostral to the lesion relates to distance from injury, laminar region, and duration of injury. The major classes of C-fiber primary afferents differed greatly in their susceptibility to structural and chemical changes and their ability to undergo plasticity. Peptidergic primary afferents showed a widespread loss throughout the dorsal horn of segments approaching the injury site. Some of this loss may have been due to decreased neuropeptide expression. The reduction in peptidergic fibers was transient, indicating compensatory sprouting and perhaps also increased neuropeptide expression within the cord. Nonpeptidergic afferents expressing GFR alpha 1 were largely unaffected by SCI. In contrast, in GFR alpha 2-expressing nonpeptidergic afferents SCI caused a permanent loss of dorsal horn innervation. Unexpectedly, GFR alpha 2 was transiently induced throughout deeper laminae but this was not due to upregulation of GFR alpha 2 in dorsal root ganglia. We also observed permanent sprouting of catecholamine terminals of supraspinal origin. This was restricted to the superficial laminae. Our results show that SCI caused a loss of sensory input as well as structural remodeling such that the balance of nociceptive inputs and descending modulation was permanently altered. These changes may contribute to mechanisms rostral to the site of SCI that trigger and maintain neuropathic pain.