Abstract

Objective To investigate the effect of intrathecal injection of minocycline on expressions of CX3C chemokine receptor 1(CX3CR1) in spinal dorsal horn of rats with NT. Methods Sixty SD rats, were randomly divided into 5 groups(n=12): normal group (Normal), nicotine withdrawal group(NT), pre-minocycline treated+nicotine withdrawal group(M+NT), nicotine withdrawal+post-minocycline treated group (NT+M), nicotine withdrawal+dimethyl sulfoxide (DMSO) group (NT+DMSO). A rat model of NT was established by subcutaneous injection of pure nicotine(3 mg/kg), three times daily for 7 d. Hyperalgesia was evaluated by observing the paw withdrawal latency(PWL). The activation of microglia was investigated by immunofluorescence staining. The expression level of CX3CR1 was studied by Western blot and immunofluorescence staining. Results The PWL of rats in NT+M group was significantly increased compared to NT group(P<0.05), but still lower than the Normal group. Compared to NT group, the expression levels of microglia and CX3CR1 in NT+M group were significantly decreased(P<0.05), but still more than Normal group (P<0.05). Conclusions Intrathecal administration of the microglia specific inhibitor minocycline can attenuate thermal hyperalgesia induced by nicotine withdrawal. Activated microglia may upregulate the expression of CX3CR1 which contribute to the development of hyperalgesia following nicotine withdrawal. Key words: Nicotine withdrawal; Hyperalgesia; CX3C chemokine receptor 1; Microglia

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