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| 1 | Spinal CCL2 Promotes Central Sensitization, Long-Term Potentiation, and Inflammatory Pain via CCR2: Further Insights into Molecular, Synaptic, and Cellular Mechanisms显示文摘Mounting evidence supports an important role of chemokines, produced by spinal cord astrocytes, in promoting central sensitization and chronic pain. In particular,CCL2(C-C motif chemokine ligand 2) has been shown to enhance N-methyl-D-aspartate(NMDA)-induced currents in spinal outer lamina Ⅱ(IIo) neurons. However, the exact molecular, synaptic, and cellular mechanisms by which CCL2 modulates central sensitization are still unclear. We found that spinal injection of the CCR2 antagonist RS504393 attenuated CCL2-and inflammation-induced hyperalgesia. Single-cell RT-PCR revealed CCR2 expression in excitatory vesicular glutamate transporter subtype2-positive(VGLUT2^+) neurons. CCL2 increased NMDAinduced currents in CCR2^+/VGLUT2+ neurons in lamina IIo; it also enhanced the synaptic NMD A currents evoked by dorsal root stimulation; and furthermore, it increased the total and synaptic NMDA currents in somatostatinexpressing excitatory neurons. Finally, intrathecal RS504393 reversed the long-term potentiation evoked in the spinal cord by C-fiber stimulation. Our findings suggest that CCL2 directly modulates synaptic plasticity in CCR2-expressing excitatory neurons in spinal lamina IIo, and this underlies the generation of central sensitization in pathological pain. | Rou-Gang Xie Yong-Jing Gao Chul-Kyu Park Ning Lu Ceng Luo Wen-Ting Wang Sheng-Xi Wu Ru-Rong Ji | 2018 | Neuroscience Bulletin2018，34，1： | 17 |
| 2 | Spinal CCL2 Promotes Pain Sensitization by Rapid Enhancement of NMDA-Induced Currents Through the ERK-GluN2B Pathway in Mouse Lamina Ⅱ Neurons显示文摘Previous studies have shown that CCL2(C-C motif chemokine ligand 2)induces chronic pain,but the exact mechanisms are still unknown.Here,we established models to explore the potential mechanisms.Behavioral experiments revealed that an antagonist of extracellular signal-regulated kinase(ERK)inhibited not only CCL2-induced inflammatory pain,but also pain responses induced by complete Freund’s adjuvant.We posed the question of the intracellular signaling cascade involved.Subsequent experiments showed that CCL2 up-regulated the expression of phosphorylated ERK(pERK)and N-methyl D-aspartate receptor[NMDAR]subtype 2B(GluN2B);meanwhile,antagonists of CCR2 and ERK effectively reversed these phenomena.Whole-cell patchclamp recordings revealed that CCL2 enhanced the NMDAR-induced currents via activating the pERK pathway,which was blocked by antagonists of GluN2B and ERK.In summary,we demonstrate that CCL2 directly interacts with CCR2 to enhance NMDAR-induced currents,eventually leading to inflammatory pain mainly through the CCL2-CCR2-pERK-GluN2B pathway. | Hui Zhang Sui-Bin Ma Yong-Jing Gao Jun-Ling Xing Hang Xian Zhen-Zhen Li Shu-Ning Shen Sheng-Xi Wu Ceng Luo Rou-Gang Xie | 2020 | Neuroscience Bulletin2020，36，11： | 3 |
| 3 | Experience type teaching to cultivate specialized nurses comprehensive ability evaluation of the effect of nursing research显示文摘 | Ceng H Jiang Z X Luo Y G | 2011 | J2011，23，14： | 1 |
| 4 | Involvement of peripheral NMDA and non-NMDA receptors in development of persistent firing of spinal wide-dynamic-range neurons induced by subcutaneous bee venom injection in the cat显示文摘 | Jun Chen Hui-Li Li Ceng Luo Zhen Li Ji-Hong Zheng | 1999 | Brain Research1999，，1： | 1 |
| 5 | Tweety-Homolog 1 Facilitates Pain via Enhancement of Nociceptor Excitability and Spinal Synaptic Transmission显示文摘Tweety-homolog 1(Ttyh1)is expressed in neural tissue and has been implicated in the generation of several brain diseases.However,its functional significance in pain processing is not understood.By disrupting the gene encoding Ttyh1,we found a loss of Ttyh1 in nociceptors and their central terminals in Ttyh1-deficient mice,along with a reduction in nociceptor excitability and synaptic transmission at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey(PAG)in the basal state.More importantly,the peripheral inflammationevoked nociceptor hyperexcitability and spinal synaptic potentiation recorded in spinal-PAG projection neurons were compromised in Ttyh1-deficient mice.Analysis of the paired-pulse ratio and miniature excitatory postsynaptic currents indicated a role of presynaptic Ttyh1 from spinal nociceptor terminals in the regulation of neurotransmitter release.Interfering with Ttyh1 specifically in nociceptors produces a comparable pain relief.Thus,in this study we demonstrated that Ttyh1 is a critical determinant of acute nociception and pain sensitization caused by peripheral inflammation. | Wen-Juan Han Sui-Bin Ma Wen-Bin Wu Fu-Dong Wang Xiu-Li Cao Dong-Hao Wang Hai-Ning Wu Rou-Gang Xie Zhen-Zhen Li Fei Wang Sheng-Xi Wu Min-Hua Zheng Ceng Luo Hua Han | 2021 | Neuroscience Bulletin2021，37，4： | 1 |
| 6 | Spatial Distribution of Parvalbumin-Positive Fibers in the Mouse Brain and Their Alterations in Mouse Models of Temporal Lobe Epilepsy and Parkinson’s Disease显示文摘Parvalbumin interneurons belong to the major types of GABAergic interneurons.Although the distribution and pathological alterations of parvalbumin interneuron somata have been widely studied,the distribution and vulnerability of the neurites and fibers extending from parvalbumin interneurons have not been detailly interrogated.Through the Cre recombinase-reporter system,we visualized parvalbumin-positive fibers and thoroughly investigated their spatial distribution in the mouse brain.We found that parvalbumin fibers are widely distributed in the brain with specific morphological characteristics in different regions,among which the cortex and thalamus exhibited the most intense parvalbumin signals.In regions such as the striatum and optic tract,even long-range thick parvalbumin projections were detected.Furthermore,in mouse models of temporal lobe epilepsy and Parkinson’s disease,parvalbumin fibers suffered both massive and subtle morphological alterations.Our study provides an overview of parvalbumin fibers in the brain and emphasizes the potential pathological implications of parvalbumin fiber alterations. | Changgeng Song Yan Zhao Jiajia Zhang Ziyi Dong Xin Kang Yuqi Pan Jinle Du Yiting Gao Haifeng Zhang Ye Xi Hui Ding Fang Kuang Wenting Wang Ceng Luo Zhengping Zhang Qinpeng Zhao Jiazhou Yang Wen Jiang Shengxi Wu Fang Gao | 2023 | Neuroscience Bulletin2023，39，11： | 0 |
| 7 | Correction:Spatial Distribution of Parvalbumin‑Positive Fibers in the Mouse Brain and Their Alterations in Mouse Models of Temporal Lobe Epilepsy and Parkinson’s Disease显示文摘In this article the wrong figure appeared as Fig.3,the figure should have appeared as shown below. | Changgeng Song Yan Zhao Jiajia Zhang Ziyi Dong Xin Kang Yuqi Pan Jinle Du Yiting Gao Haifeng Zhang Ye Xi Hui Ding Fang Kuang Wenting Wang Ceng Luo Zhengping Zhang Qinpeng Zhao Jiazhou Yang Wen Jiang Shengxi Wu Fang Gao | 2023 | Neuroscience Bulletin2023，39，11： | 0 |
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