Alterations in the BDNF–mTOR Signaling Pathway in the Spinal Cord Contribute to Hyperalgesia in a Rodent Model of Chronic Restraint Stress

摘要: Abstract Stress is a non-specific, systemic, physiological response of the body to strong internal and external environmental stimuli. Accumulating evidence has suggested that stress, particularly chronic restraint stress (CRS), can reduce pain threshold increase sensitivity. However, pathogenic therapeutic mechanisms underlying CRS remain unclear. Here, we aimed investigate roles brain-derived neurotrophic factor (BDNF)–mammalian target rapamycin (mTOR) signaling pathway in CRS-induced abnormal was successfully mimicked 7 days after model development, paw withdrawal mechanical (PWMT) tail-flick latency (TFL) were evaluated. significantly altered BDNF mTOR phosphorylation anterior cingulate cortex spinal cord but not hippocampus. On day 7, single dose 7,8-dihydroxyflavone, an activator BDNF–tropomyosin receptor kinase B, administered via intraperitoneal or intrathecal injection. Notably, only injection improved PWMT TFL. Additionally, rapamycin, inhibitor, failed induce any behavioral changes, whereas In conclusion, sensitivity, probably by altering BDNF–mTOR cord.