B1 and TRPV-1 receptor genes and their relationship to hyperalgesia following spinal cord injury
B1 and TRPV-1 receptor genes and their relationship to hyperalgesia following spinal cord injury
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DOI：
10.1097/01.brs.0000245865.97424.b4
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发表时间：
2006-11-15
期刊：
影响因子：
3
通讯作者：
Resnick, Daniel K.
中科院分区：
文献类型：
--
作者：
DomBourian, Melkon G.;Turner, Nicholas A.;Resnick, Daniel K.
研究设计.脊髓损伤后疼痛行为的实验室研究。探讨大鼠脊髓损伤（SCI）后脊髓伤害性感受基因表达的变化及其与疼痛行为表现的关系。SCI后的神经性疼痛是常见的，致残的，并且在很大程度上无法治疗。在周围神经损伤模型中，缓激肽B1和香草素1（TRPV-1）受体活性与神经病理性疼痛行为相关。我们试图研究这些基因产物在SCI介导的疼痛中的作用。使用MAS-CIS撞击器对大鼠进行SCI。使用后肢退缩潜伏期试验，在损伤前和损伤后定期测试动物热痛觉过敏的出现。B1和TRPV-1基因的表达采用实时聚合酶链反应进行评估。免疫组化法检测B1和TRPV-1受体在脊髓内的分布。与未表现出痛觉过敏的SCI动物相比，在表现出痛觉过敏的脊髓损伤区域检测到B1和TRPV-1基因表达的两倍以上增加。免疫组化染色显示，这两种受体类型主要定位于背角。与假手术对照组相比，所有损伤动物的TRPV-1受体染色减少，而B1受体染色增加。B1和TRPV-1受体基因在SCI后表现出热痛觉过敏的动物的损伤脊髓中过表达，与没有痛觉过敏的类似损伤动物相比。这一发现与过去关于这些受体在伤害感受中的作用的研究一致，并表明脊髓中正在发生导致临床疼痛综合征的可改变过程。
Study Design. Laboratory investigation of pain behavior following spinal cord injury.Objective. To explore changes in the spinal cord expression of nociceptive genes following spinal cord injury (SCI) as they relate to the manifestation of pain behavior in rats.Summary of Background Data. Neuropathic pain following SCI is common, disabling, and largely untreatable. In peripheral nerve injury models, bradykinin B1 and vanilloid 1 (TRPV-1) receptor activity is associated with neuropathic pain behavior. We sought to examine the role of these gene products in SCI-mediated pain.Methods. Rats were subjected to SCI using the MAS-CIS impactor. Animals were tested preinjury and at regular intervals postinjury for the appearance of thermal hyperalgesia using a hind limb withdrawal latency test. The expression of B1 and TRPV-1 genes was assessed using real-time polymerase chain reaction. Immunohistochemistry was used to localize the B1 and TRPV-1 receptors within the spinal cord.Results. Greater than twofold increases in the expression of the B1 and TRPV-1 genes were detected in the injured region of the spinal cord in animals exhibiting hyperalgesia compared with animals with SCI that did not display hyperalgesia. Immunohistochemical staining revealed that both receptor types were largely localized to the dorsal horn. Staining for TRPV-1 receptors decreased while that for B1 receptors increased in all of the injured animals when compared with sham-operated controls.Conclusion. B1 and TRPV-1 receptor genes are over-expressed in the injured spinal cord of animals manifesting thermal hyperalgesia following SCI compared with similarly injured animals without hyperalgesia. This finding is consistent with past work regarding the role of these receptors in nociception and indicates that ongoing modifiable processes are occurring in the spinal cord that lead to clinical pain syndromes.