PMID- 23918351 OWN - NLM STAT- MEDLINE DCOM- 20140528 LR - 20130916 IS - 1097-4547 (Electronic) IS - 0360-4012 (Linking) VI - 91 IP - 10 DP - 2013 Oct TI - Brain-derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat. PG - 1312-21 LID - 10.1002/jnr.23254 [doi] AB - The facet joint is commonly associated with neck and low back pain and is susceptible to loading-induced injury. Although tensile loading of the cervical facet joint has been associated with inflammation and neuronal hyperexcitability, the mechanisms of joint loading-induced pain remain unknown. Altered brain-derived neurotrophic factor (BDNF) levels are associated with a host of painful conditions, but the role of BDNF in loading-induced joint pain remains undefined. Separate groups of rats underwent a painful cervical facet joint distraction or a sham procedure. Bilateral forepaw mechanical hypersensitivity was assessed and BDNF mRNA and protein levels were quantified in the dorsal root ganglion (DRG) and spinal cord at days 1 and 7. Facet joint distraction induced significant (P < 0.001) mechanical hypersensitivity at both time points. Painful joint distraction did not alter BDNF mRNA in the DRG compared with sham levels but did significantly increase (P < 0.016) BDNF protein expression over sham in the DRG at day 7. Painful distraction also significantly increased BDNF mRNA (P = 0.031) and protein expression (P = 0.047) over sham responses in the spinal cord at day 7. In a separate study, intrathecal administration of the BDNF-sequestering molecule trkB-Fc on day 5 after injury partially attenuated behavioral sensitivity after joint distraction and reduced pERK in the spinal cord at day 7 (P < 0.045). Changes in BDNF after painful facet joint injury and the effect of spinal BDNF sequestration in partially reducing pain suggest that BDNF signaling contributes to the maintenance of loading-induced facet pain but that additional cellular responses are also likely involved. CI - Copyright (c) 2013 Wiley Periodicals, Inc. FAU - Kras, Jeffrey V AU - Kras JV AD - Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania. FAU - Weisshaar, Christine L AU - Weisshaar CL FAU - Quindlen, Julia AU - Quindlen J FAU - Winkelstein, Beth A AU - Winkelstein BA LA - eng GR - AR056288/AR/NIAMS NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20130806 PL - United States TA - J Neurosci Res JT - Journal of neuroscience research JID - 7600111 RN - 0 (Brain-Derived Neurotrophic Factor) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/*metabolism MH - Cervical Vertebrae MH - Disease Models, Animal MH - Ganglia, Spinal/*metabolism MH - Hyperalgesia/metabolism/physiopathology MH - Male MH - Pain/*metabolism/physiopathology MH - Rats MH - Rats, Sprague-Dawley MH - Reverse Transcriptase Polymerase Chain Reaction MH - Signal Transduction/physiology MH - Spinal Cord/*metabolism MH - Up-Regulation MH - Zygapophyseal Joint/*injuries OTO - NOTNLM OT - BDNF OT - ERK OT - facet joint OT - pain OT - trkB EDAT- 2013/08/07 06:00 MHDA- 2014/05/29 06:00 CRDT- 2013/08/07 06:00 PHST- 2013/02/19 00:00 [received] PHST- 2013/04/26 00:00 [revised] PHST- 2013/04/30 00:00 [accepted] PHST- 2013/08/07 06:00 [entrez] PHST- 2013/08/07 06:00 [pubmed] PHST- 2014/05/29 06:00 [medline] AID - 10.1002/jnr.23254 [doi] PST - ppublish SO - J Neurosci Res. 2013 Oct;91(10):1312-21. doi: 10.1002/jnr.23254. Epub 2013 Aug 6.