PMID- 28579944
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1662-5102 (Print)
IS  - 1662-5102 (Electronic)
IS  - 1662-5102 (Linking)
VI  - 11
DP  - 2017
TI  - Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating 
      Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats 
      with Neuropathic Pain.
PG  - 145
LID - 10.3389/fncel.2017.00145 [doi]
LID - 145
AB  - 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 mug/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 depression-induced hypoalgesia.
FAU - Wei, Xiao
AU  - Wei X
AD  - Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of 
      SciencesBeijing, China.
FAU - Sun, Yuqi
AU  - Sun Y
AD  - Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of 
      SciencesBeijing, China.
AD  - Department of Psychology, University of Chinese Academy of SciencesBeijing, 
      China.
FAU - Luo, Fei
AU  - Luo F
AD  - Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of 
      SciencesBeijing, China.
AD  - Department of Psychology, University of Chinese Academy of SciencesBeijing, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20170519
PL  - Switzerland
TA  - Front Cell Neurosci
JT  - Frontiers in cellular neuroscience
JID - 101477935
PMC - PMC5437111
OTO - NOTNLM
OT  - depression
OT  - dexamethasone
OT  - glucocorticoid receptor
OT  - neuropathic pain
OT  - spinal dorsal horn
EDAT- 2017/06/06 06:00
MHDA- 2017/06/06 06:01
PMCR- 2017/01/01
CRDT- 2017/06/06 06:00
PHST- 2017/02/17 00:00 [received]
PHST- 2017/05/03 00:00 [accepted]
PHST- 2017/06/06 06:00 [entrez]
PHST- 2017/06/06 06:00 [pubmed]
PHST- 2017/06/06 06:01 [medline]
PHST- 2017/01/01 00:00 [pmc-release]
AID - 10.3389/fncel.2017.00145 [doi]
PST - epublish
SO  - Front Cell Neurosci. 2017 May 19;11:145. doi: 10.3389/fncel.2017.00145. 
      eCollection 2017.