Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord

IF 2 Q3 NEUROSCIENCES IBRO Neuroscience Reports Pub Date : 2024-10-24 DOI:10.1016/j.ibneur.2024.10.002
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Abstract

Perioperative Paradoxical sleep deprivation (PSD) is associated with postoperative hyperalgesia. However, the clinical therapeutic strategies for PSD-induced postoperative hyperalgesia are limited. Electroacupuncture (EA) has been used for attenuating many types of pain, including neuropathic pain and inflammatory pain, but its effect on PSD-induced postoperative hyperalgesia is still unclear, and its analgesia mechanism should be further explored. In this study, we designed to investigate the possible mechanism of PSD-induced postoperative hyperalgesia and the effect of EA on PSD-induced postoperative hyperalgesia, and whether the mechanism is related to the BDNF/TrkB signaling pathway mediated by α7nAChR in the spinal cord. The paw withdrawal thermal latency (PWTL) and paw withdrawal mechanical threshold (PWMT) of rats were used to detect PSD-induced hyperalgesia. The expression of α7nAChR, BDNF, TrkB and KCC2 in the spinal cord were evaluated by Western blot and immunofluorescence. The results showed that preoperative 24 h PSD significantly decreased the PWTL and PWMT. The expression of α7nAChR and KCC2 significantly downregulated in the spinal cord of PSD-induced postoperative hyperalgesia rats, the opposite was observed for BDNF and TrkB expression. Moreover, intrathecal injection of alpha-bungarotoxin (α-BGT), a selective antagonist for α7nAChR, not only aggravated the pain hypersensitivity, but also demonstrated a further decrease of α7nAChR and KCC2 expression and a further increase of BDNF and TrkB expression. EA stimulation increased the PWTL and PWMT values of PSD-induced postoperative hyperalgesia rats, significantly upregulated α7nAChR and KCC2 expression, and significantly downregulated BDNF and TrkB expression. Moreover, intrathecal injection of α-BGT suppressed the analgesic effect of EA, inhibited the enhancement of α7nAChR and KCC2 expression and the reduction of BDNF and TrkB expression induced by EA. In conclusion, our study indicated that 24 h PSD can cause postoperative hyperalgesia, and the mechanism may be related to the disorder of α7nAChR mediated BDNF/TrkB-KCC2 signaling pathway. EA can alleviate postoperative hyperalgesia induced by PSD, which may be related to its effect in activating α7nAChR, inhibiting the expression of BDNF/TrkB, and up-regulating the expression of KCC2 in the spinal cord.
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电针通过a7nAChR介导的脊髓BDNF/TrkB-KCC2信号通路缓解矛盾性睡眠剥夺诱导的术后痛觉减退
围手术期矛盾性睡眠剥夺(PSD)与术后痛觉减退有关。然而,针对 PSD 引起的术后痛觉减退的临床治疗策略十分有限。电针(EA)已被用于减轻多种类型的疼痛,包括神经性疼痛和炎症性疼痛,但其对 PSD 引起的术后痛觉减退的作用尚不明确,其镇痛机制有待进一步探讨。本研究旨在探讨PSD诱导术后痛觉减退的可能机制及EA对PSD诱导术后痛觉减退的影响,以及该机制是否与脊髓中α7nAChR介导的BDNF/TrkB信号通路有关。实验采用大鼠爪退热潜伏期(PWTL)和爪退机械阈值(PWMT)来检测PSD诱导的痛觉减退。通过Western印迹和免疫荧光评估了α7nAChR、BDNF、TrkB和KCC2在脊髓中的表达。结果表明,术前 24 小时 PSD 可明显降低 PWTL 和 PWMT。α7nAChR和KCC2在PSD诱导的术后痛觉减退大鼠脊髓中的表达明显下调,而BDNF和TrkB的表达则相反。此外,鞘内注射α-bungarotoxin(α-BGT)--一种α7nAChR的选择性拮抗剂,不仅会加重痛觉过敏,而且会进一步降低α7nAChR和KCC2的表达,进一步提高BDNF和TrkB的表达。EA刺激增加了PSD诱导的术后痛觉减退大鼠的PWTL和PWMT值,显著上调了α7nAChR和KCC2的表达,并显著下调了BDNF和TrkB的表达。此外,鞘内注射 α-BGT 可抑制 EA 的镇痛作用,抑制 EA 诱导的 α7nAChR 和 KCC2 表达的增强以及 BDNF 和 TrkB 表达的降低。总之,我们的研究表明,24 h PSD可引起术后痛觉减退,其机制可能与α7nAChR介导的BDNF/TrkB-KCC2信号通路紊乱有关。EA 可减轻 PSD 引起的术后痛感,这可能与其激活脊髓中的α7nAChR、抑制 BDNF/TrkB 的表达和上调 KCC2 的表达有关。
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来源期刊
IBRO Neuroscience Reports
IBRO Neuroscience Reports Neuroscience-Neuroscience (all)
CiteScore
2.80
自引率
0.00%
发文量
99
审稿时长
14 weeks
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