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Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain
Wei, Xiao1; Sun, Yuqi1,2; Luo, Fei1,2
2017-05-19
发表期刊FRONTIERS IN CELLULAR NEUROSCIENCE
ISSN1662-5102
文章类型Article
卷号11期号:0页码:1-16
摘要

Although depression-induced altered pain perception has been described in several laboratory and clinical studies, its neurobiological mechanism in the central nervous system (CNS), particularly in the spinal dorsal horn, remains unclear. Therefore, in this study, we aimed to clarify whether nociceptive sensitivity of neuropathic pain is altered in the olfactory bulbectomy (OB) model of depression and whether glucocorticoid receptor (GR), which is involved in the etio-pathologic mechanisms of both major depression and neuropathic pain, contributes to these processes in the spinal dorsal horn of male Sprague-Dawley rats. The results showed that mechanical allodynia and thermal hyperalgesia induced by spinal nerve ligation (SNL) were attenuated in OB-SNL rats with decreased spinal GR expression and nuclear translocation, whereas non-olfactory bulbectomy (NOB)-SNL rats showed increased spinal GR nuclear translocation. In addition, decreased GR nuclear translocation with normal mechanical nociception and hypoalgesia of thermal nociception were observed in OB-Sham rats. Intrathecal injection (i. t.) of GR agonist dexamethasone (Dex; 4 m g/rat/day for 1 week) eliminated the attenuating effect of depression on nociceptive hypersensitivity in OB-SNL rats and aggravated neuropathic pain in NOB-SNL rats, which was associated with the up-regulation of brain-derived neurotrophic factor (BDNF), TrkB and NR2B expression in the spinal dorsal horn. The present study shows that depression attenuates the mechanical allodynia and thermal hyperalgesia of neuropathic pain and suggests that altered spinal GR-BDNF-TrkB signaling may be one of the reasons for depressioninduced hypoalgesia.

关键词glucocorticoid receptor depression neuropathic pain dexamethasone spinal dorsal horn
DOI10.3389/fncel.2017.00145
收录类别SCI
语种英语
项目资助者National Natural Science Foundation of China (NSFC)(31500857) ; China Postdoctoral Science Foundation(2015M570166 ; NSFC(31171067 ; Key laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences ; 2016T90145) ; 31471061)
WOS研究方向Neurosciences & Neurology
WOS类目Neurosciences
WOS记录号WOS:000403297700001
WOS标题词Science & Technology ; Life Sciences & Biomedicine
关键词[WOS]OLFACTORY BULBECTOMIZED RATS ; PERIPHERAL-NERVE INJURY ; NEUROTROPHIC FACTOR ; GENE-EXPRESSION ; FKBP5 EXPRESSION ; MAJOR DEPRESSION ; NMDA RECEPTORS ; ANIMAL-MODEL ; ACTIVATION ; BEHAVIOR
引用统计
被引频次:1[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/21534
专题中国科学院心理健康重点实验室
作者单位1.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, Beijing, Peoples R China
2.Univ Chinese Acad Sci, Dept Psychol, Beijing, Peoples R China
推荐引用方式
GB/T 7714
Wei, Xiao,Sun, Yuqi,Luo, Fei. Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain[J]. FRONTIERS IN CELLULAR NEUROSCIENCE,2017,11(0):1-16.
APA Wei, Xiao,Sun, Yuqi,&Luo, Fei.(2017).Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain.FRONTIERS IN CELLULAR NEUROSCIENCE,11(0),1-16.
MLA Wei, Xiao,et al."Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain".FRONTIERS IN CELLULAR NEUROSCIENCE 11.0(2017):1-16.
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