Zhou Q Q, Chen S S, Zhang Q Q, Liu P F, Fang H Z, Yang Y, Zhang L C
Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical University, Xuzhou, Jiangsu Province, China.
Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou Medical University, Xuzhou, Jiangsu Province, China.
Braz J Med Biol Res. 2017 Aug 7;50(9):e6275. doi: 10.1590/1414-431X20176275.
Increasing evidence suggests that the cerebrospinal fluid-contacting nucleus (CSF-contacting nucleus) mediates the transduction and regulation of pain signals. However, the precise molecular mechanisms remain unclear. Studies show that release of fractalkine (FKN) from neurons plays a critical role in nerve injury-related pain. We tested the hypothesis that release of FKN from the CSF-contacting nucleus regulates neuropathic pain, in a chronic constriction injury rat model. The results show that FKN is expressed by neurons, via expression of its only receptor CX3CR1 in the microglia. The levels of soluble FKN (sFKN) were markedly upregulated along with the increase in FKN mRNA level in rats subjected to chronic constriction injury. In addition, injection of FKN-neutralizing antibody into the lateral ventricle alleviated neuropathic pain-related behavior followed by reduction in microglial activation in the CSF-contacting nucleus. The results indicate that inhibition of FKN release by the CSF-contacting nucleus may ameliorate neuropathic pain clinically.
越来越多的证据表明，脑脊液接触核介导疼痛信号的转导和调节。然而，确切的分子机制仍不清楚。研究表明，神经元释放的 fractalkine（FKN）在神经损伤相关疼痛中起关键作用。我们在慢性压迫损伤大鼠模型中测试了脑脊液接触核释放 FKN 调节神经性疼痛的假说。结果表明，FKN 由神经元表达，通过其在小胶质细胞中唯一的受体 CX3CR1 表达。在慢性压迫损伤的大鼠中，可溶性 FKN（sFKN）水平随着 FKN mRNA 水平的增加而显著上调。此外，向侧脑室注射 FKN 中和抗体可减轻神经性疼痛相关行为，随后脑脊液接触核中的小胶质细胞活化减少。结果表明，脑脊液接触核对 FKN 释放的抑制可能在临床上改善神经性疼痛。
