CX3CR1 Mediates Nicotine Withdrawal-Induced Hyperalgesia via Microglial P38 MAPK Signaling

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• 作者：Yonghong Ding ; Wenhui Shi ; Guannan Xie ; Ailan Yu ; Qinghe Wang…
• 关键词：Nicotine withdrawal ; Hyperalgesia ; CX3CR1 ; Microglia ; p38 MAP kinase
• 刊名：Neurochemical Research
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：40
• 期：11
• 页码：2252-2261
• 全文大小：8,480 KB
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• 作者单位：Yonghong Ding (1) (2) (3)
  Wenhui Shi (1) (2)
  Guannan Xie (3)
  Ailan Yu (3)
  Qinghe Wang (1) (2)
  Zongwang Zhang (1) (2) (3)
  
  1. Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou, 221000, Jiangsu, People’s Republic of China
  2. Jiangsu Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou, 221000, Jiangsu, People’s Republic of China
  3. Department of Anesthesiology, Liaocheng People’s Hospital, No. 67 Dongchang West Road, Liaocheng City, 252000, Shandong, People’s Republic of China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Previously, we reported that nicotine withdrawal (NT) significantly increased pain sensitivity in rats. Recent reports suggest that fractalkine is involved in the spinal cord neuron-to-microglia activation via CX3CR1 signaling. However, its contribution to NT-induced hyperalgesia and the underlying mechanisms have yet to be elucidated. In the present study, a rat model of NT was used to test the changes in CX3CR1 expression in the spinal cord. We also evaluated the effect of the CX3CR1 neutralizing antibody on spinal microglial activity, the expression of phosphorylated p38-mitogen-activated protein kinase (p-p38-MAPK) and heat-induced pain responses. We established a NT model via subcutaneous injection of pure nicotine (3 mg/kg), three times daily for 7 days. The expression of CX3CR1 was studied by Western blot and immunofluorescence staining. Following NT, the rats received daily intrathecal injections of CX3CR1 neutralizing antibody for 3 days. The change in paw withdrawal latency (PWL) was observed. The activation of microglia and the expression of p-p38-MAPK were investigated by Western blot and immunofluorescence staining. The expression of CX3CR1 was significantly increased after NT and co-localized with IBA-1. NT rats treated with CX3CR1 neutralizing antibody showed significantly increased PWL on day 4 after NT. Furthermore, the activation of microglia and the expression of p-p38-MAPK in the spinal cord were suppressed. These results indicate that microglial CX3CR1/p38MAPK pathway is critical for the development of pain hypersensitivity after NT.