| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5736284 | Brain Research Bulletin | 2017 | 64 Pages |
Abstract
Our results demonstrate that GFRα3 knockdown specially inhibits cold hyperalgesia following CCI via decreasing the expression level and plasma membrane trafficking of TRPM8 in DRG. GFRα3 and its downstream mediator, TRPM8, represent a new analgesia axis which can be further exploited in sensitized cold reflex under the condition of chronic pain.
Keywords
EGFRCFATRPA1DRGTrpdsRNAPWTPC12TRPM8PWLCCIdorsal root ganglioncomplete Freund’s adjuvantSmall interfering RNAdouble-stranded RNAsiRNApaw withdrawal thresholdchronic constriction injurypaw withdrawal latencyNeuropathic painpheochromocytoma cellstransient receptor potential melastatin 8Cold hyperalgesiatransient receptor potentialtransient receptor potential ankyrin 1Epidermal growth factor receptor
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Authors
Lin Su, Ruichen Shu, Chengcheng Song, Yonghao Yu, Guolin Wang, Yazhuo Li, Changxiao Liu,