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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Receptor for activated C kinase 1 mediates the chronic constriction injury-induced neuropathic pain in the rats' peripheral and central nervous system
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Receptor for activated C kinase 1 mediates the chronic constriction injury-induced neuropathic pain in the rats' peripheral and central nervous system

机译：活化C激酶1的受体介导大鼠外周和中枢神经系统中的慢性收缩损伤诱导的神经性疼痛

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摘要

Peripheral and central sensitization has been reported as significant features in the course of the occurrence and development of neuropathic pain (NP). Receptor for activated C kinase 1 (RACK1), a scaffold protein, participated in fundamental cellular activities and various neuronal functions. Peripheral and central sensitization are a state that the morphology of neuronal cell bodies as well as the corresponding function change, whether this process can be regulated by RACK1 is still unknown. In this study, the biological effects and mechanisms of RACK1 contributes to the pathogenesis of chronic constriction injury (CCI)-induced neuropathic pain were investigated. By western blot and staining, we found that RACK1 protein changed in dorsal root ganglion (DRG) neurons and spinal cord (SC) neurons except glial cells after CCI. Especially, RACK1 was co-located with IB4-, CGRP-positive neurons, suggesting it was related to integrate nociceptive information from the primary aff;erents in DRG. The successful establishment of CCI models also directly led to mechanical allodynia and heat hyperalgesia, which could be reversed by intrathecal injection of RACK1 siRNA. Furthermore, intrathecal injection of RACK1 siRNA reduced the expression of RACK1 and accompanying spinal c-fos, which is the transcription factor and marker of neuronal activation. These results suggested that targeting RACK1 be a sensible approach for treating NP.
机译：外周和中央致敏在神经病疼痛（NP）的发生和发展过程中被报告为重要特征。活化的C激酶1（Rack1）的受体，支架蛋白质，参与基本细胞活性和各种神经元功能。外围和中央致敏是神经元细胞体的形态以及相应的功能改变的状态，无论该过程是否可以由Rack1调节仍然未知。在这项研究中，Rack1的生物学效应和机制有助于慢性收缩损伤的发病机制（CCI） - 诱导的神经性疼痛。通过蛋白质印迹和染色，我们发现CCI之后的胶质细胞除了胶质细胞外的背根神经节（DRG）神经元（DRG）神经元（DRG）神经元和脊髓（SC）神经元中发生变化。特别是，Rack1与IB4-，CGRP阳性神经元共同定位，这表明它与从主要作用中整合伤害性信息;在DRG中的最佳。成功建立CCI模型也直接导致机械异常和热痛觉过敏，这可以通过鞘内注射rack1 siRNA来逆转。此外，鞘内注射Rack1 siRNA降低了Rack1和伴随脊柱C-FOS的表达，这是神经元激活的转录因子和标志物。这些结果表明，靶向Rack1是治疗NP的明智方法。

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