Chronic pain after clip-compression injury of the rat spinal cord
Chronic pain after clip-compression injury of the rat spinal cord
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DOI：
10.1006/exnr.2002.8026
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发表时间：
2002-11-01
影响因子：
5.3
通讯作者：
Weaver, LC
中科院分区：
文献类型：
--
作者：
Bruce, JC;Oatway, MA;Weaver, LC
慢性触觉异常性疼痛和痛觉过敏是脊髓损伤（SCI）常见的并发症，其机制尚不清楚。可能的原因是伤害性和非伤害性初级感觉神经元的中枢动脉的可塑性变化以及下行调节性多巴胺能通路的变化。一个临床相关的夹压缩模型的SCI在大鼠被用来研究慢性疼痛的假定机制。行为测试（n = 18只大鼠）表明，在第12胸椎节段（T-12）的中度（35 g）或重度（50 g）SCI可靠地产生慢性触觉异常性疼痛和痛觉过敏，可以从后爪和背部诱发。定量形态测定（n = 37）显示，脊髓损伤后，胸腰段T-6至L-4内初级感觉神经元的Abeta-，Adelta-和C-纤维中枢动脉的密度或分布没有变化。这一观察结果排除了疼痛相关行为与中枢传入乔木分布或密度变化之间的强制性关系。背角5-羟色胺免疫反应性区域（n = 12）在损伤部位尾侧（L1-4）减少，在其吻侧（T9-11）增加3倍。5-羟色胺的减少和损伤尾部触觉异常性疼痛和痛觉过敏的存在与调节疼痛传递的下行抗伤害性神经元能束的中断一致。5-羟色胺在吻段增加的功能意义可能与触觉异常性疼痛的发展有关，因为5-羟色胺也具有已知的亲伤害性作用。下降的多巴胺能通路的变化需要进一步的研究，因为损伤部位的头侧和尾侧多巴胺能输入平衡的破坏可能导致SCI后慢性疼痛的病因。(C)2002 Elsevier Science（美国）。
Chronic tactile allodynia and hyperalgesia are frequent complications of spinal cord injury (SCI) with poorly understood mechanisms. Possible causes are plastic changes in the central arbors of nociceptive and nonnociceptive primary sensory neurons and changes in descending modulatory serotonergic pathways. A clinically relevant clip-compression model of SCI in the rat was used to investigate putative mechanisms of chronic pain. Behavioral testing (n = 18 rats) demonstrated that moderate (35 g) or severe (50 g) SCI at the 12th thoracic spinal segment (T-12) reliably produces chronic tactile allodynia and hyperalgesia that can be evoked from the hindpaws and back. Quantitative morphometry (n = 37) revealed no changes after SCI in the density or distribution of Abeta-, Adelta-, and C-fiber central arbors of primary sensory neurons within the thoracolumbar segments T-6 to L-4. This observation rules out a mandatory relationship between pain-related behaviors and changes in the distribution or density of central afferent arbors. The area of serotonin immunoreactivity in the dorsal horn (n = 12) decreased caudal to the injury site (L1-4) and increased threefold rostral to it (T9-11). The decreased serotonin and presence of tactile allodynia and hyperalgesia caudal to the injury are consistent with disruption of descending antinociceptive serotonergic tracts that modulate pain transmission. The functional significance of the increased serotonin in rostral segments may relate to the development of tactile allodynia as serotonin also has known pronociceptive actions. Changes in the descending serotonergic pathway require further investigation, as a disruption of the balance of serotonergic input rostral and caudal to the injury site may contribute to the etiology of chronic pain after SCI. (C) 2002 Elsevier Science (USA).