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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
Source PublicationFRONTIERS IN CELLULAR NEUROSCIENCE
ISSN1662-5102
SubtypeArticle
Volume11Issue:0Pages:1-16
Abstract

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.

Keywordglucocorticoid receptor depression neuropathic pain dexamethasone spinal dorsal horn
DOI10.3389/fncel.2017.00145
Indexed BySCI
Language英语
Funding OrganizationNational 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 Research AreaNeurosciences & Neurology
WOS SubjectNeurosciences
WOS IDWOS:000403297700001
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
WOS KeywordOLFACTORY BULBECTOMIZED RATS ; PERIPHERAL-NERVE INJURY ; NEUROTROPHIC FACTOR ; GENE-EXPRESSION ; FKBP5 EXPRESSION ; MAJOR DEPRESSION ; NMDA RECEPTORS ; ANIMAL-MODEL ; ACTIVATION ; BEHAVIOR
Citation statistics
Cited Times:3[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.psych.ac.cn/handle/311026/21534
Collection中国科学院心理健康重点实验室
Affiliation1.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, Beijing, Peoples R China
2.Univ Chinese Acad Sci, Dept Psychol, Beijing, Peoples R China
First Author AffilicationKey Laboratory of Mental Health, CAS
Recommended Citation
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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