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检索条件"任意字段=第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议"

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Electrical Stimulation Reduces Smokers' Craving by Modulating the Coupling between DLPFC and Parahippocampal Gyrus

Electrical Stimulation Reduces Smokers' Craving by Modulatin...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Li-Zhuang Yang Bin Shi Wei Zhang Feng Gu Ying Wang Ying Liu Xiaochu Zhang Key Laboratory of Brain Function and Disease Chinese Academy of SciencesSchool of Life SciencesUniversity of Science & Technology of China Provincial Hospital Affiliated to Anhui Medical University School of Humanities & Social Science University of Science & Technology of China Center of Medical Physics and Technology Hefei Institutes of Physical ScienceCAS Centers for Biomedical Engineering University of Science & Technology of China

Applying transcranial direct current stimulation(t DCS) over dorsal lateral prefrontal cortex(DLPFC) can reduce cue-elicited craving in smokers. However, the underlying neural mechanism is not clear. We hypothesized that 1) t DCS over DLPFC can enhance the coupling between DLPFC and brain regions related with smoking cue reactivity;2) the alteration in functional connectivity can even be manifested in the intrinsic properties of the brain. Nineteen male smokers attended the present study. Participants received the La Rc(anode: left DLPFC, cathode: right DLPFC, 1m A of 30 minutes) or sham stimulation in each session. A total of 3 f MRI scans were acquired within each session, including the go/no-go task, the resting state fM RI, and the smoking-cue attention bias task(AB). The smoking cue-elicited craving was reduced in the La Rc condition compared with the sham condition. The whole brain analysis on task-based f MRI revealed significant t DCS effect in the go/no-go and AB task. In the go/no-go task, stimulating DLPFC reduce activations in cognitive control systems such as DLPFC and the inferior parietal lobe(IPL). The main effect of t DCS was also revealed in the right superior temporal gyrus in the AB task. Three brain regions showed specific reactivity to smoking-cue, including superior frontal gyrus(SFG), and bilateral Parahippocampal gyrus(PHG). Psychophysical interaction analysis(PPI) analysis revealed that the functional coupling between bilateral PHG and DLPFC were modulated by tD CS. Besides, the resting state functional connectivity analysis(rs-fc) revealed that those alterations in functional coupling could also manifested in the resting state brain network. The present study supports the viewpoint that the local function of DLPFC can be enhanced by t DCS. Moreover, we show that t DCS over DLPFC modulates the functional coupling between DLPFC and bilateral PHG, suggesting that electrical stimulation may help smokers regulate involuntary memory retrieval of

关键词： tDCS,smoking,craving,DLPFC,fMRI

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Up-regulation of belta4 subunit of large-conductance Ca2+-activated potassium channels contributes to anxiety-like behaviors in the anterior cingulate cortex

Up-regulation of belta4 subunit of large-conductance Ca2+-ac...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Huan Zhao shichao Han Fancheng Meng Ming Zhang Hui Xu Department of Neurobiology and Collaborative Innovation Center for Brain Science School of Basic MedicineFourth Military Medical University Center for Neuron and Disease Frontier Institute of Science and TechnologyXi’an Jiaotong University

The large-conductance Ca2+- and voltage-gated K+ channels or BK channels are ubiquitously expressed throughout the central nervous system including the cingulate cortex and contribute to action potential repolarization and fast afterhyperpolarization(f AHP), both of which influence firing rates at the neuronal cells and neurotransmitter release through some Ca2+ transients. It has been found that a significant reduction in BK channels expression in the amygdala of mice accompanied anxiety-like behavior. However, little has been known about the expression of BK channel subunits that modify the channel's properties in the anterior cingulate cortex(ACC). In our present study, BK-mediated f AHP was altered in ACC pyramidal neurons accompanied anxiety-like behavior in the m CCD rat. With the method of whole-cell patch-clamp method, the amplitude of f AHP was reduced and the AP duration was increased in pyramidal neurons which induce the hyperexcitability of ACC neurons accompanied anxiety-like behavior. NS1619(10μM),an opener of BK channels,significantly rescued the alteration of f AHP and AP duration in ACC pyramidal neurons in the m CCD rat. Meanwhile, by bath-applied the BK channels inhibitor iberiotoxin(IBTX,100 nM) the f AHP was reduced and the APduration was increased in ACC pyramidal neurons of the sham rat. ACC neurons of the anxious animals revealed a pronounced reduction in the BK currents in the m CCD rats compared with the sham rats. Interestingly, we did not find reduction in BK channel expression in ACC of m CCD rats, while a significant increase of accessory belta4 subunit of BK channel expression in the ACC accompanied anxiety-like behavior in the m CCD rat by using RT-PCR and Western blotting. These data demonstrate that the belta4 subunit is related to reduction of the BK channels' function and that anxiety-like behavior induced by chronic pain could at least partly be explained by up-regulation in the belta4 subunit of BK channels in the ACC.

关键词： large-conductance Ca2+-activated potassium channel belta4 subunit anxiety excitability anterior cingulate cortex

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Role of Locus Coeruleus Circuit in Mediating Resilience to Social Stress

Role of Locus Coeruleus Circuit in Mediating Resilience to S...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Hongxing Zhang Dipesh Chaudhury Barbara Juarez Allyson K.Friedman Stacy M.Ku Erin S.Calipari Alexander R.Nectow Marshall Crumiller Cheng Jiang Haosheng Sun Jeffrey M.Friedman Jun-Li Cao Ming-Hu Han Department of Pharmacology and Systems Therapeutics Icahn school of Medicine at Mount Sinai Jiangsu Province Key Laboratory of Anesthesiology Xuzhou Medical College Fishberg Department of Neuroscience Friedman Brain InstituteIcahn school of Medicine at Mount Sinai Laboratory of Molecular Genetics Howard Hughes Medical InstituteThe Rockefeller University Laboratory of Biophysics The Rockefeller University

Our previous work, using the chronic social defeat stress model of depression, shows that the resilience phenotype is associated with the stable firing activity of ventral tegmental area(VTA) dopamine neurons in the brain's reward circuitry. This stable firing status is established through the homeostatic balance between the excitatory hyperpolarization-activated cation channel current(Ih) and inhibitory potassium(K+) channel currents(Friedman AK et al., Science, 2014). In the present study, utilizing multiple retrograde labeling techniques, we investigated the in vitro firing activities of locus coeruleus(LC) neurons specifically projecting to the VTA(LC-VTA) in control, susceptible and resilient mice. Unexpectedly, we observed that LC-VTA neurons fired significantly higher in the resilient subgroup as compared to control, while LC-VTA neurons from susceptible mice had a firing activity comparable to that of control mice. Consistently, our in vivo recordings from intact anesthetized animals showed that LC neurons of resilient mice exhibited higher firing rates and significantly increased phasic firing events as compared to control and susceptible mice. Furthermore, chronic(20 minutes per day for 5-10 days), butnot acute(5 minutes during social interaction test), optogenetic activation of LC-VTA neurons in susceptible mice reversed social avoidance behavior, suggesting that activating LC-VTA neural circuit promotes the resilient phenotype. Additional recording studies from these neurons showed that optogenetic activation of the LC-VTA neurons in susceptible mice increased excitatory Ih and inhibitory K+ currents in VTA dopamine neurons, as seen in the resilient subgroup. This suggests that the norepinephrine released from LC may contribute to the stabilization of VTA dopamine neurons in the resilience phenotype. Moreover, utilizing a circuit-mapping molecular profiling technique(Ekstrand MI, Nectow AR et al., Cell, 2014), we found that VTA-NAc dopamine neurons expre

关键词： VTA Role of Locus Coeruleus Circuit in Mediating Resilience to Social Stress

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The genetics of Parkinson's Disease

The genetics of Parkinson's Disease

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Beisha Tang Department of Neurology Xiangya HospitalCentral South University State Key Laboratory of Medical Genetics Hunan Province Key Laboratory of Neurodegenerative Disorders Parkinson's Disease Center Beijing Institute for Brain DisordersCapital University of Medical Sciences

Parkinson's disease(PD) is the second most common neurodegenerative disorder nowadays, which is clinically characterized by resting tremor, bradykinesia, rigidity, postural instability and a positive response to dopamine replacement therapy. The classic pathological findings of PD are the loss of dopaminergic neurons and cytoplasm inclusions of aggregated proteins Lewy bodies. The specific mechanism of PD is still not very clear;it is associated with aging, environmental and genetic factors, and genetics have been paid more and more attentions. In our preliminary studies, we found that Parkin mutations are the most commonly identified genetic variations in Chinese patients with AREP(48.3%) or EOP(12.6%). Mutations in the PINK1, DJ-1, and PLA2G6 genes were also found in cases of AREP(6.9%, 3.4%, 3.4%, respectively) and sporadic EOP(3.1%, 2.4%, 0.79%, respectively). Thus far, no pathogenic mutations have been detected in the ATP13A2 and FBXO7 genes in the Chinese population. In our study, sixteen SNPs located in the 8 genes and/or loci(SNCA, LRRK2, MAPT, GBA, HLA-DR, BST1, PARK16, and PARK17) were analyzed in a Chinese cohort consisting of 1061 well-characterized PD patients and 1066 control subjects from Central South of China's mainland. We found that Rep1, rs356165, and rs11931074 in SNCA gene;G2385 R in LRRK2 gene;rs4698412 in BST1 gene;rs1564282 in PARK17;and L444 P in GBA gene were associated with PD with adjustment of sex and age(p < 0.05) in the analysis of 16 variants. PD risk increased when Rep1 and rs11931074, G2385 R, rs1564282, rs4698412;rs11931074 and G2385 R, rs1564282, rs4698412;G2385 R and rs1564282, rs4698412;and rs1564282 and rs4698412 were combined for the association analysis. In addition, PD risk increased cumulatively with the increasing number of variants(odds ratio for carrying 3 variants, 3.494). We sequenced the exomes of EOPD families to depict the de novo mutational paradigm for PD. We found the probands are enriched in nonsynonymous and l

关键词： Parkinson,genetics,early-onset parkinson' disease,gene,SNP

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Moderate alcohol preconditioning activates neuronal BKCa channels to protect brain damage-induced by cerebral ischemia and reperfusion

Moderate alcohol preconditioning activates neuronal BKCa cha...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Yi-Long Zhao Fang Su Wei-Wei Li An-Chen Guo Yong-Jun Wang Qun Wang Department of Neurology Beijing Tiantan HospitalCapital Medical University Beijing Key Laboratory of Translational Medicine for Cardiovascular Diseases Beijing Institute for Brain Disorder

Objective Stroke is the third most common cause of death after heart attack and cancer and has profound negative social and economic effects. Because clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. The results of a large number of epidemiologic studies indicate that consumption of red wine at low to moderate levels is cardioprotective and neuroprotective, reducing the incidence and severity of myocardial infarction and stroke. Studies conducted in cultured cell and intact animal models attributed these beneficial effects to "Ethanol preconditioning". Ethanol preconditioning(Et OH-PC) refers to a phenomenon in which tissues are protected from the deleterious effects of ischemia/reperfusion(I/R) by prior ingestion of ethanol at low to moderate levels. Recent studies have shown that activation of large conductance calcium activated potassium channels(BKCa) plays a key role in the protection of cerebral protection with moderate alcohol preconditioning. Thus, we propose the following hypothesis: moderate alcohol preconditioning activates neuronal BKCa channels to protect brain damage-induced by cerebral ischemia and reperfusion. In this experiment, we use cerebral ischemia reperfusion model to clarify this viewpoint through pharmacological intervention of BKCa channel agonist(NS11021, NS) and inhibitor(Paxilline, PX).Methods The SD rat were randomly divided into the following six groups(n=10):Sham,Ischemia?reperfusion(I/R),Et OH-PC+I/R,NS11021-PC+I/R,Paxilline+Et OH-PC+I/R,Paxilline+NS11021-PC+I/R. The volume of 95% ethanol to be instilled(in μL) was calculated as follows: [body weight(g)×0.6] + 0.3. This volume of ethanol was mixed in 0.3m L of sterile distilled water just before administration to the animals by gavage. Both Et OH-PC and NS11021-PC(0.1mg/kg;ip) were induced 24 h before I?R. The Paxilline(2.5mg/kg;ip) was administered 10 min

关键词： ethanol preconditioning neuroprotection cerebral ischemia/reperfusion BKCa channels

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Differential regulation of GSK3β in spinal dorsal horn and in hippocampus contributes to neuropathic pain and memory deficits following peripheral nerve injury

Differential regulation of GSK3β in spinal dorsal horn and ...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Xiao Wei Wen-Shan Gui Yong-Yong Li Li-Jun Zhou Xian-Guo Liu Pain Research Center and Department of Physiology Zhongshan School of Medicine of Sun Yat-sen University

Objective Glycogen synthase kinase 3β(GSK3β) inhibitor is proposed as an attractive candidate for the treatment of cognitive deficit, while its effect on neuropathic pain is not clear. Measures With use of behavioral tests and molecular biological techniques, the role of GSK3β and its downstream molecules in short term memory(STM) and neuropathic pain in spared nerve injury(SNI) model was evaluated. Results GSK3β activity was reduced in spinal dorsal horn(SDH) but enhanced in hippocampus following SNI. Inhibition of GSK3β by SB216763(5mg/kg, i.p.) injected 1h before and 3, 6, and 9d after surgery rescued STM deficit caused by SNI, but induced mechanical allodynia, a behavioral signs of neuropathic pain, in sham-operated rats. Furthermore, we found that β-catenin, a downstream molecule of GSK-3β, and BDNF were upregulated in SDH but downregulated in hippocampus after SNI. Importantly, injection of SB216763 also upregulated β-catenin and BDNF in SDH, while reversed the downregulation of β-catenin and BDNF in hippocampus produced by SNI. The results suggested that SNI might upregulate and downregulate BDNF in SDH and hippocampus by differential regulation of β-catenin. Indeed, β-catenin transcription inhibitor i CRT 14(50mg/kg, i.p.) injected 3h before and 3, 6 and 9d after surgery inhibited BDNF expression in both SDH and hippocampus and prevented SNI-induced mechanicalallodynia but led to STM deficit in na?ve C57 mice. Microglial inhibitor minocycline(i.p. 50mg/kg, bid) injected 1d before to 7d after surgery or specific deletion of microglia with Mac-1 SAP(i.t. 8ug/rat 3d before surgery) prevented the neuropathic pain, STM deficit and differential regulation of GSK3β/β-catenin/BDNF signaling produced by SNI. Conclusion The results demonstrated that the decrease and increase in activity of GSK3β in SDH and in hippocampus led to neuropathic pain and memory deficit, respectively. Treatment of cognitive deficit with GSK3β inhibitor may lead to neuropathic pain.

关键词： neuropathic pain short-term memory deficits glycogen synthase kinase 3β β-catenin brain-derived neurotrophic factor microglia

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A new algorithm using maximum distributed energy to calculate baseline to automatically detect high frequency oscillations in epilepsy

A new algorithm using maximum distributed energy to calculat...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Guo-Ping Ren Jia-Qing Yan Zhi-Xin Yu Dan Wang Shan-Shan Mei Xiao-Li Li Yun-Lin Li Xiao-Fei Wang Xiao-Feng Yang Neuroelectrophysiological Laboratory Xuanwu HospitalCapital Medical University Center of Epilepsy Beijing Institute for Brain Disorders Institute of Electrical Engineering Yanshan University Functional Neurology and Neurosurgery Haidian Hospital State Key Laboratory of Cognitive Neuroscience and Learning IDG/McGovern Institute for Brain ResearchBeijing Normal University Center for Collaboration and Innovation in Brain and Learning Sciences Beijing Normal University Department of Neruology Beijing Children's HospitalCapital Medical University

High frequency oscillations(HFOs) on i EEG is a promising candidate biomarker for defining the epileptogenic zone. Visual marking of HFOs is highly time consuming and subjective. Therefore, identifying accurate automatic HFO detectors is necessary to provide greater insight into the features and clinical values of HFOs. Most existing automatic detectors use solid-state baseline computing methods, so they perform well in channels with rare HFOs but lose accuracy in very active channels. To address this problem, we propose a new algorithm for using the method of maximum distributed energy to calculate dynamic baseline to improve the accuracy of HFOs detection in both inactive and active channels. Human i EEG data was collected from 6 patients with refractory epilepsy. Recordings were collected with a sample rate of 2000 Hz. We randomly chose 30 channels, and from each channel we selected a 5-minute segment during slow wave sleep for analysis. Two experienced EEG analysts visually identified and marked "ripple" HFOs separately. To determine inter-rater concordance, Cohen's Kappa coefficient was computed(κ> 0.5). Activity identified by both EEG analysts as "ripple" HFOs was considered the gold standard for true HFOs. After visual marking, the automatic detector was applied. The i EEG data were band-passed between 80-200 Hz. We then calculated the absolute value of amplitude of the filtered signal and classified all points in the segment by quality threshold clustering(QTC). Points with similar energy levels were grouped into the same category. The biggest category contained the most points and had the largest distributed energy. We concluded that the points in the maximum distribution area were baseline points, and we then calculated the baseline amplitude by taking the mean amplitude of these points. Because baselines can change slightly over time, we set up a 5 second moving window. When the window moved, the baseline changed according to the signal inside the window,

关键词： high frequency oscillations automatic detector,biomarker,epileptogenic zone

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NAc shell Arc/Arg3.1 protein mediates reconsolidation of morphine CPP by increase GluR1 cell surface expression:activation of ERK coupled CREB is required

NAc shell Arc/Arg3.1 protein mediates reconsolidation of mor...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Xiu-Fang Lv Lin-Lin Sun Meng Jia Cai-Lian Cui Ji-Sheng Han Neuroscience Research Institute Peking University Department of Neurobiology School of Basic Medical SciencesPeking University Key Laboratory for Neuroscience of the Ministry of Education and the Ministry of Public Health Basic Medical Research Centre Medical School of Nantong University

Relapse into drug abuse evoked by re-exposure to the drug-associated context has been a primary problem in treatment of drug addiction. Disrupting the reconsolidation of drug-related context memory would therefore limit the relapse susceptibility. However, little has been known about whether Arc/Arg3.1 can mediate reconsolidation of morphine CPP via Glu R1-ERK-p CREB signaling. First, we assessed Arc/Arg3.1 and correlative molecule expression in the NAc shell during the reconsolidation of morphine CPP. The retrieval of morphine CPP in rats specifically increased Arc/Arg3.1 protein level in the NAc shell, accompanied simultaneously by increase in phosphorylation of extracellular signal-regulated kinase1/2(p ERK1/2), phosphorylation of c AMP response element-binding(p CREB), and up-regulation of membrane α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors(AMPARs) Glu R1 subunit level. Then we demonstrated that intra-NAc shell infusion U0126, an inhibitor of the ERK kinase MEK, immediately after retrieval of morphine CPP prevented the retrieval-induced up-regulation of p ERK1/2, p CREB, Arc/Arg3.1 and membrane Glu R1. The effect of disrupting the reconsolidation of morphine CPP by U0126 could last for at least 14 days, and could not be evoked by a priming injection of morphine. Furthermore, specific knockdown of Arc/Arg3.1 in the NAc shell decreased membrane Glu R1 level, and impaired both the reconsolidation and the reinstatement of morphine CPP. These result suggested that NAc shell mediates the reconsolidation of morphine-associated context memory via up-regulating the level of membrane of Glu R1, and in which the activation of ERK-CREB signal pathway in local, as an upstream mechanism of Arc/Arg3.1, is required.

关键词： Arc/Arg3.1 conditioned place preference(CPP) reconsolidation ERK pCREB GluR1

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Activation of mGluR4 attenuates oxidative stress-induced death of neural stem cells through inhibition of JNK and P38 MAPK signaling

Activation of mGluR4 attenuates oxidative stress-induced dea...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Xinlin Chen Zhichao Zhang Wen Ma Li Wang Hanshi Gong Yumei Tian Jianshui Zhang Jianxin Liu Haixia Lu Yong Liu Institute of Neurobiology Xi’an Jiaotong University Health Science Center Department of Obstetrics and Gynecology The Affiliated Hospital of Xi'an Medical College Xi’an Mental Health Center

Objective Neural stem cell(NSC) replacement promises a novel therapeutic strategy for stroke and other brain diseases. However, this approach is impeded possibly due to the hostile brain environments which result in massive cell death. A high oxidative stress status in vivo caused by damaged brain, essentially accounting for the harsh brain microenvironments, makes a crucially challenge to survival of the resided as well as transplanted NSCs. Hence,conferring antioxidative properties to NSCs may contribute to the potential strategies in favor to combating existing oxidative stimulus. Type 4 metabotropic glutamate receptor(m Glu R4) is a member of group III m Glu Rs, which belong to family C G-protein coupled receptors in inhibiting adenylate cyclase(AC) activity in heterologous expression systems. Although an experiment suggested that an m Glu R4 ligand, phosphoserine(P-Ser) may improve survival of rat embryonic cortex-derived neural progenitors in normal condition, it is unknown if m Glu R4 plays a role in protection NSCs from oxidative injury. These previous findings prompt the potential of m Glu R4 as a drugtarget in NSC replacement therapy, which could enhance neurogenic fate commitment of NSCs and/or protects these cells against the insults of harsh CNS microenvironments. Here we attempt to disclose the contribution of m Glu R4 to the neuroprotection against oxidative stress-induced NSC death and related cells signaling pathways. Methods(1) Cell culture: Rats NSCs were prepared from E15.5 cortex and propagated into neurospheres in serum-free DMEM/F12(1:1) supplemented with 2% B27, 1% N2, 10 ng/ml b FGF and 2.5μg/ml heparin.(2) Oxidative stress on NSCs was experimentally induced by adding H2O2, and MTT assay was used to optimize the oxidative injury condition and the concentration of VU0155041 for conducting the experiment. 3. PI/Hoechst and TUNEL staining were used to observe cell viability and apoptosis. *** of m Glu R4: we designed two target sequence

关键词： metabotropic glutamate receptor 4 neural stem cells oxidative stress hydrogen peroxide apoptosis

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Upregulation of chemokine CXCL12 in the dorsal root ganglia and spinal cord contributes to the development and maintenance of neuropathic pain following spared nerve injury in rats

Upregulation of chemokine CXCL12 in the dorsal root ganglia ...

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第六届亚太神经科学联合会学术会议暨中国神经科学学会第十一届全国学术会议

作者： Li-Ying BAI Jun-Liang QIAN Dong-Xiao DUAN Su-Fang LIU Wei Zhang Ji-Tian XU Department of Physiology & Neurobiology Medical School of Zhengzhou University Department of Anesthesiology The First Affiliated HospitalZhengzhou University

Objective: Emerging evidence indicates that CXCL12/CXCR4 signaling is involved in chronic pain. However, few studies have systemically assessed the role of this signaling in direct nerve injury-induced neuropathic pain and the associated underlying mechanism. The present study is to elucidate the signaling mechanism of CXCL12-mediated neuropathic pain. Methods: The spared nerve injury(SNI) in rats was used as pain model to induce neuropathic pain. The pain-related behaviors were tested by "up-down" method. The expressions of CXCL12, CXCR4(a cognate receptor of CXCL12), TNF-α and the phosphorylation level of ERK in lumbar 5 dorsal root ganglia(DRG) and spinal cord dorsal horn were measured by western blot, immunofluorescence staining orELSA. A procedure of intrathecal injection of AMD3100 and CXCL12-neutralized antibody was used to verify the role of CXCL12/CXCR4 signaling in SNI-induced neuropathic pain. Results: In the present study, we determined that SNI resulted in an increased expression of CXCL12 and its cognate receptor CXCR4 in L5 DRG neurons and satellite glial cells. SNI also induced long-lasting upregulations of CXCL12 and CXCR4 in the ipsilateral L4-5 spinal cord dorsal horn, which was characterized by CXCL12 expression in neurons and CXCR4 expression that colocalized with neurons and astrocytes. Moreover, SNI induced a sustained increase in the expression of TNF-α in the DRG and spinal cord. Intraperitoneal injection(i.p.) of the TNF-α-synthesis inhibitor thalidomide reduced SNI-induced mechanical hypersensitivity and inhibited the expression of CXCL12 in the DRG and spinal cord. Intrathecal injection(i.t.) of the CXCR4 antagonist AMD3100, both 30 min before and seven days after SNI, resulted in reductions of behavioral signs of allodynia. Rats treated with i.t. or i.p. boli of AMD3100 on the eighth day of SNI exhibited attenuated abnormal pain behaviors. The neuropathic pain that was established following SNI was also impaired by the i.t. administratio

关键词： Spared nerve injury CXCL12,TNF-α Neuropathic pain Extracellular signal-regulated kinase Spinal cord

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