Involvement of CX3CL1/CX3CR1 signaling in spinal long term potentiation.
Involvement of CX3CL1/CX3CR1 signaling in spinal long term potentiation.
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CX3CL1/CX3CR1 信号传导参与脊髓长时程增强。
DOI：
10.1371/journal.pone.0118842
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Lü N
中科院分区：
文献类型：
--
作者：
Bian C;Zhao ZQ;Zhang YQ;Lü N
脊髓C纤维诱发场电位的长时程增强（LTP）被认为是脊髓中枢敏感化的基本机制。越来越多的证据表明脊髓小胶质细胞在脊髓LTP和病理性疼痛中的作用。作为神经元-小胶质细胞相互作用的关键信号，CX 3CL 1/CX 3CR 1信号通路在病理性疼痛中的作用也被广泛研究。本研究探讨了CX 3CL 1/CX 3CR 1信号转导是否在脊髓LTP中发挥作用。结果表明，10串强直刺激（100 Hz，2s）坐骨神经（TSS）在脊髓背角产生明显的C纤维诱发场电位LTP，持续时间超过3 h。用抗CX 3CR 1中和抗体（CX 3CR 1 AB）阻断CX 3CL 1/CX 3CR 1信号传导显著抑制TSS诱导的LTP。外源性CX 3CL 1显著增强3-trains TSS诱导的大鼠LTP。TSS（100 Hz，1 s，4 trains）可诱发C57 BL/6野生型小鼠脊髓C纤维诱发电位LTP。然而，在CX 3CR 1-/-小鼠中，TSS未能诱导LTP和行为超敏反应，证实了CX 3CR 1在脊髓LTP诱导中的重要作用。此外，用IL-18 BP或抗IL-23中和抗体（IL-23 AB）阻断CX 3CL 1/CX 3CR 1信号转导的潜在下游因子IL-18或IL-23，可明显抑制大鼠脊髓LTP。这些结果表明，CX 3CL 1/CX 3CR 1信号参与了啮齿动物脊髓背角C纤维诱发场电位的LTP。
The long-term potentiation (LTP) of spinal C-fiber-evoked field potentials is considered as a fundamental mechanism of central sensitization in the spinal cord. Accumulating evidence has showed the contribution of spinal microglia to spinal LTP and pathological pain. As a key signaling of neurons-microglia interactions, the involvement of CX3CL1/CX3CR1 signaling in pathological pain has also been investigated extensively. The present study examined whether CX3CL1/CX3CR1 signaling plays a role in spinal LTP. The results showed that 10-trains tetanic stimulation (100 Hz, 2s) of the sciatic nerve (TSS) produced a significant LTP of C-fiber-evoked field potentials lasting for over 3 h in the rat spinal dorsal horn. Blockade of CX3CL1/CX3CR1 signaling with an anti-CX3CR1 neutralizing antibody (CX3CR1 AB) markedly suppressed TSS-induced LTP. Exogenous CX3CL1 significantly potentiated 3-trains TSS-induced LTP in rats. Consistently, spinal LTP of C-fiber-evoked field potentials was also induced by TSS (100 Hz, 1s, 4 trains) in all C57BL/6 wild type (WT) mice. However, in CX3CR1-/- mice, TSS failed to induce LTP and behavioral hypersensitivity, confirming an essential role of CX3CR1 in spinal LTP induction. Furthermore, blockade of IL-18 or IL-23, the potential downstream factors of CX3CL1/CX3CR1 signaling, with IL-18 BP or anti-IL-23 neutralizing antibody (IL-23 AB), obviously suppressed spinal LTP in rats. These results suggest that CX3CL1/CX3CR1 signaling is involved in LTP of C-fiber-evoked field potentials in the rodent spinal dorsal horn.
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