目的  观察不同时间点神经痛小鼠海马CA3区外周单核细胞的浸润，阐述这一现象对小鼠神经痛及焦虑样行为的影响。 方法  采用健康雄性C57小鼠，将小鼠随机分为假手术组（sham）、坐骨神经分支选择性损伤（SNI）模型组（SNI）、CCR2抑制剂RS102895处理组（SNI+RS102895）和小胶质细胞活化抑制剂米诺环素（MC）处理组（SNI+MC），共4组。其中假手术组和模型组均进一步分为7 d 、14 d 和18 d 组，SNI+RS102895和SNI+ MC 组均在第18天时取材。手术诱发神经痛，采用机械缩足阈（PWTs）测定不同时点痛阈，所有小鼠处死前2 d进行高架十字迷宫(EPM)实验，处死前1 d进行旷场实验(OFT)观察焦虑样行为变化。免疫荧光法检测小鼠海马CA3脑区白细胞分化抗原45（CD45）的表达及与小胶质细胞标记物离子钙接头蛋白分子1（IBA-1）、跨膜蛋白119（TMEM119），星形胶质细胞标记物胶质纤维酸性蛋白(GFAP)和神经元标记物神经元核抗原（NeuN）的共表达，流式细胞术检测14 d SNI小鼠全脑单核细胞的百分比。18 d 小鼠 SNI 后第5~16天分别灌胃给予MC 90 mg/（kg·d)、RS102895 5 mg/（kg·d）与生理盐水，观察阻断单核细胞浸润对小鼠神经痛、焦虑样行为及海马CA3区CD45及IBA-1的表达的影响。 结果  7 d和14 d组小鼠SNI 后1 d PWTs下降，持续到处死前（P<0.01）。假手术组CD45表达极少；与同时段假手术组比较，7 d SNI 小鼠CD45表达无增加（P>0.05），14 d SNI小鼠CD45表达显著上升（P<0.01），且只与IBA1和TMEM119有少量共表达，与GFAP、NeuN无共表达。14 d SNI小鼠全脑单核细胞百分比显著上升（P<0.01）。抑制小胶质细胞激活与抑制CCR2表达均能减少SNI小鼠CA3区CD45的表达（P<0.01），且能提高SNI小鼠机械痛阈（P<0.01）并缓解焦虑样行为（P<0.01）。 结论  SNI诱发神经痛14 d后小鼠海马CA3区有外周单核细胞的浸润，该现象可能参与了神经痛的维持及促进焦虑样行为的发生。 

Objective  To investigate the infiltration of peripheral monocyte in the hippocampal CA3 area in neuralgia mice at different time points and explore the effects of the infiltration on neuralgia and the neuralgia-induced anxiety-like behavior in mice. Methods  The healthy male C57 mice were randomly divided into four groups: sham, sciatic nerve branch selective injury（SNI）model （SNI）, CCR2 inhibitor RS102895 (SNI + RS102895) and microglial inhibitor minocycline (MC) (SNI + MC) groups. Both the sham and SNI groups were further divided into 7 days, 14 days and 18 days groups, and the SNI + RS102895 and SNI + MC groups were sampled on the 18th day. Neuralgia was induced by SNI, and mechanical hyperalgesia was assessed by paw withdrawal threshold (PWTs) at different time points. Elevated plus maze (EPM) and open field test (OFT) were performed respectively two days and one day before sacrifice. Immunofluorescence was used to observe the expressions of leukocyte differentiation antigen 45 (CD45) and the co-expression with microglial markers ionized calcium binding adaptor molecule-1(IBA-1), transmembrane protein 119 (TMEM119), astrocyte marker glial fibrillary acidic protein (GFAP), and neuronal marker neuronal nuclei (NeuN) in the hippocampal CA3. The percentage of monocytes in the whole brain of 14 days SNI mice was determined by flow cytometry. Minocycline at 90 mg/(kg·d),  RS102895 at 5 mg/(kg·d) and saline were administered orally on the 5th to 16th day in the corresponding 18 days groups, and the effects of blocking monocyte infiltration on neuralgia and anxiety-like behavior and the expressions of CD45 and IBA-1 in CA3 region of hippocampus were observed.  Results  On the first day after SNI, the PWTs of mice in the 7 days and 14 days groups decreased and continued until before sacrifice( P< 0.01). The CD45 expression did little in the 7 days sham group. Compared with the sham group at the same time point, the CD45 expression did not increase in 7 days SNI mice (P>0.05) and increased significantly in 14 days SNI mice ( P <0.01), only slightly co-expressed with IBA-1 and TMEM119 and no co-expression with GFAP and NeuN, the percentage of monocytes in the whole brain increased significantly in 14 days SNI mice ( P<0.01). Inhibition of microglial activation or CCR2 expression reduced the expression of CD45 in the CA3 in SNI mice (P <0.01), increased the PWTs ( P <0.01) and alleviated anxiety-like behavior in SNI mice (P<0.01).  Conclusion  There was an infiltration of peripheral monocytes in the hippocampal CA3 region after 14 days of SNI-induced neuralgia, which might be involved in the maintenance of neuralgia and the development of neuralgia-induced anxiety-like behaviors.