Battlefield Pain Management Research Group, United States Army Institute of Surgical Research, 3698 Chambers Pass, JBSA Fort Sam Houston, San Antonio, TX, 78234-4504, USA.
BMC Neurosci. 2019 Apr 24;20(1):17. doi: 10.1186/s12868-019-0500-1.
Reports 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.
Unstressed 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).
These results indicate that BDNF-TrkB signaling in PFC and hypothalamus contributes to CIS-induced exacerbated mechanical allodynia in thermal injury state.
有报道称,受伤前的应激事件会加重受伤后的疼痛。应激引起的热痛增高的机制尚不清楚。在这里,我们研究了慢性间歇性应激(CIS)对有和没有热损伤的大鼠前额叶皮层(PFC)和下丘脑的伤害感受行为和脑源性神经营养因子(BDNF)系统的影响。
未应激的大鼠在应激暴露期间表现出短暂的机械性痛觉过敏。有热损伤的应激大鼠表现出持续加剧的机械性痛觉过敏(P<0.001)。有热损伤的应激大鼠的 PFC 中 BDNF mRNA 的表达增加(P<0.05),下丘脑 TrkB 和 p-TrkB(P<0.05)蛋白水平升高,但单独应激或热损伤的大鼠则没有。此外,CTX-B 的给药显著减轻了热损伤大鼠的应激诱导的机械性痛觉过敏(P<0.001)。
这些结果表明,PFC 和下丘脑的 BDNF-TrkB 信号通路参与了 CIS 诱导的热损伤状态下机械性痛觉过敏的加剧。