Abstract | BACKGROUND: OBJECTIVE: To investigate the role of α7nAChR in CM and provide a new therapeutic target for CM. MATERIALS AND METHODS: Thirty-six male Sprague-Dawley rats were distributed randomly into control, CM, PNU-282987, and α-bungarotoxin groups (n=9 rats in each group). The CM model was established by the recurrent daily administration of inflammatory soup on the dura over the course of 1 week. The hind paw threshold and facial allodynia were assessed by the von Frey test. The expression levels of α7nAChR, tumor necrosis factor-alpha, and interleukin-1 beta were analyzed by Western blot and real-time fluorescence quantitative polymerase chain reaction. The location of α7nAChR in the hippocampus was quantified by immunofluorescence, as well as the microglial and astrocyte alterations. Changes in the calcitonin gene-related peptide and the phosphorylated JNK protein among different groups were measured by Western blot. RESULTS: We found that the expression of α7nAChR was reduced after repeated inflammatory soup administration. The increased expression of tumor necrosis factor-alpha, interleukin-1 beta, and calcitonin gene-related peptide in CM group were significantly decreased by PNU-282987 and aggravated by α-bungarotoxin. Moreover, PNU-282987 decreased the numbers of astrocytes and microglia compared with the numbers in the CM group in both hippocampal CA1 and CA3 regions. In contrast, α-bungarotoxin activated the astrocytes and microglia, but the differences with respect to the CM group were not significant. Activated c-Jun N-terminal kinase signaling was observed in CM rats and was also blocked by PNU-282987. CONCLUSION:
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Authors | Qing Liu, Chaoyang Liu, Li Jiang, Maolin Li, Ting Long, Wei He, Guangcheng Qin, Lixue Chen, Jiying Zhou |
Journal | Journal of pain research
(J Pain Res)
Vol. 11
Pg. 1129-1140
( 2018)
ISSN: 1178-7090 [Print] New Zealand |
PMID | 29942148
(Publication Type: Journal Article)
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