Involvement of brain-derived neurotrophic factor (BDNF) in chronic intermittent stress-induced enhanced mechanical allodynia in a rat model of burn pain

被引:16
|
作者
Sosanya, Natasha M. [1 ]
Garza, Thomas H. [1 ]
Stacey, Winfred [1 ]
Crimmins, Stephen L. [1 ]
Christy, Robert J. [1 ]
Cheppudira, Bopaiah P. [1 ]
机构
[1] US Army Inst Surg Res, Battlefield Pain Management Res Grp, 3698 Chambers Pass, San Antonio, TX 78234 USA
关键词
Chronic intermittent stress; Thermal injury; Mechanical allodynia; BDNF; TrkB; p-TrkB; Cyclotraxin-B; CHRONIC PSYCHOLOGICAL STRESS; ADOLESCENT SOCIAL STRESS; ANXIETY-LIKE BEHAVIOR; CHRONIC MILD STRESS; NEUROPATHIC PAIN; PREFRONTAL CORTEX; COLD ALLODYNIA; UP-REGULATION; EXPRESSION; INFLAMMATION;
D O I
10.1186/s12868-019-0500-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
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页数:18
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