BackgroundReports show that stressful events before injury exacerbates post-injury pain. The mechanism underlying stress-induced heightened thermal pain is unclear. Here, we examined the effects of chronic intermittent stress (CIS) on nociceptive behaviors and brain-derived nerve growth factor (BDNF) system in the prefrontal cortex (PFC) and hypothalamus of rats with and without thermal injury.ResultsUnstressed rats showed transient mechanical allodynia during stress exposure. Stressed rats with thermal injury displayed persistent exacerbated mechanical allodynia (P < 0.001). Increased expression of BDNF mRNA in the PFC (P < 0.05), and elevated TrkB and p-TrkB (P < 0.05) protein levels in the hypothalamus were observed in stressed rats with thermal injury but not in stressed or thermally injured rats alone. Furthermore, administration of CTX-B significantly reduced stress-induced exacerbated mechanical allodynia in thermally injured rats (P < 0.001).ConclusionThese results indicate that BDNF-TrkB signaling in PFC and hypothalamus contributes to CIS-induced exacerbated mechanical allodynia in thermal injury state.

中文翻译：

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脑源性神经营养因子（BDNF）参与慢性间歇性应激诱导的烧伤大鼠模型机械性异常性疼痛

背景报告显示，受伤前的压力事件会加剧受伤后的疼痛。压力引起的热痛加剧的机制尚不清楚。在这里，我们研究了慢性间歇性压力 (CIS) 对有和没有热损伤的大鼠的前额叶皮层 (PFC) 和下丘脑的伤害性行为和脑源性神经生长因子 (BDNF) 系统的影响。在压力暴露期间。具有热损伤的应激大鼠表现出持续加剧的机械异常性疼痛（P < 0.001）。在有热损伤的应激大鼠中观察到 PFC 中 BDNF mRNA 的表达增加（P < 0.05），下丘脑中的 TrkB 和 p-TrkB 蛋白水平升高（P < 0.05），但在单独的应激或热损伤大鼠中没有观察到。此外，