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Bilateral activation of glial cells and cellular distribution of the chemokine CCL2 and its receptor CCR2 in the trigeminal subnucleus caudalis of trigeminal neuropathic pain model.
Histochemistry and Cell Biology ( IF 2.3 ) Pub Date : 2020-02-04 , DOI: 10.1007/s00418-020-01850-4
Lucie Kubíčková 1 , Ilona Klusáková 1 , Petr Dubový 1
Affiliation  

Glial cells activated by peripheral nerve injury contribute to the induction and maintenance of neuropathic pain by releasing neuromodulating cytokines and chemokines. We investigated the activation of microglia and astrocytes as well as the cellular distribution of the chemokine CCL2 and its receptor CCR2 in the trigeminal subnucleus caudalis (TSC) ipsilateral and contralateral to infraorbital nerve ligature (IONL). The left infraorbital nerve was ligated under aseptic conditions, and sham controls were operated without nerve ligature. Tactile hypersensitivity was significantly increased bilaterally in vibrissal pads of both sham- and IONL-operated animals from day 1 to 7 and tended to normalize in sham controls surviving for 14 days. Activated microglial cells significantly increased bilaterally in the TSC of both sham- and IONL-operated animals with a marked but gradual increase in the ipsilateral TSC from 1 to 7 days followed by a decrease by day 14. In contrast, robust activation of astrocytes was found bilaterally in the TSC of IONL-operated rats from 3 to 14 days with a transient activation in the ipsilateral TSC of sham-operated animals. Cellular distribution of CCL2 varied with survival time. CCL2 immunofluorescence was detected in neurons within 3 days and in astrocytes at later time points. In contrast, CCR2 was found only in astrocytes at all time points with CCR2 intensity being dominant in the ipsilateral TSC. In summary, our results reveal bilateral activation of microglial cells and astrocytes as well as changes in the cellular distribution of CCL2 and its receptor CCR2 in the TSC during the development and maintenance of orofacial neuropathic pain.

中文翻译:

三叉神经痛模型的三叉神经尾核中胶质细胞的双向激活和趋化因子CCL2及其受体CCR2的细胞分布。

周围神经损伤激活的神经胶质细胞通过释放神经调节细胞因子和趋化因子而有助于神经性疼痛的诱导和维持。我们调查了小胶质细胞和星形胶质细胞的激活以及趋化因子CCL2及其受体CCR2在三叉神经尾核(TSC)同侧和对侧眶下神经结扎(IONL)的细胞分布。在无菌条件下结扎左眶下神经,并在无神经结扎的情况下进行假手术。从第1天到第7天,假手术和IONL手术动物的触感垫的双侧触觉超敏性均显着增加,并且在存活14天的假对照中趋于正常。在假手术和IONL手术的动物的TSC中,活化的小胶质细胞在两侧均显着增加,同侧TSC从1天到7天显着但逐渐增加,然后在第14天逐渐减少。相反,发现星形胶质细胞的强烈活化在IONL手术大鼠的TSC中双侧进行3到14天的实验,在假手术动物的同侧TSC中进行短暂激活。CCL2的细胞分布随生存时间而变化。3天之内在神经元中检测到CCL2免疫荧光,随后的时间点在星形胶质细胞中检测到。相反,CCR2在所有时间点仅在星形胶质细胞中发现,CCR2强度在同侧TSC中占主导地位。综上所述,
更新日期:2020-04-21
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