Abstract | BACKGROUND: METHODS: RESULTS: CFA injection into rat hindpaw resulted in mechanical hyperalgesia and significant increases in levels of TNF-α in the inflamed tissues, along with enhancement of BDNF and trkB receptor as well as the pain mediators CGRP and transient receptor potential vanilloid receptor subtype 1 (TRPV1) in DRG. Direct injection of TNF-α into rat hindpaw resulted in similar effects with retrograde transport of TNF-α along the saphenous nerve to DRG during CFA-induced inflammation. Primary DRG cultures chronically treated with TNF-α showed significant enhancement of mRNA and protein levels of BDNF and trkB receptor, BDNF release and trkB-induced phospho-ERK1/2 signal. Moreover, CGRP and substance P release were enhanced in DRG cultures after chronic TNF-α treatment or acute BDNF stimulation. In addition, we found that BDNF up-regulated trkB expression in DRG cultures. CONCLUSIONS: Based on our current experimental results, we conclude that inflammation and TNF-α up-regulate the BDNF-trkB system in DRG. This phenomenon suggests that up-regulation of BDNF in DRG may, in addition to its post-synaptic effect in spinal dorsal horn, act as an autocrine and/or paracrine signal to activate the pre-synaptic trkB receptor and regulate synaptic excitability in pain transmission, thereby contributing to the development of hyperalgesia.
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Authors | Ya-Tin Lin, Long-Sun Ro, Hung-Li Wang, Jin-Chung Chen |
Journal | Journal of neuroinflammation
(J Neuroinflammation)
Vol. 8
Pg. 126
(Sep 30 2011)
ISSN: 1742-2094 [Electronic] England |
PMID | 21958434
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Brain-Derived Neurotrophic Factor
- TRPV Cation Channels
- Trpv1 protein, rat
- Tumor Necrosis Factor-alpha
- Substance P
- Receptor, trkB
- Calcitonin Gene-Related Peptide
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Topics |
- Animals
- Brain-Derived Neurotrophic Factor
(genetics, metabolism)
- Calcitonin Gene-Related Peptide
(genetics, metabolism)
- Cells, Cultured
- Ganglia, Spinal
(cytology, drug effects, physiology)
- Hyperalgesia
(metabolism)
- Inflammation
(chemically induced, immunology)
- MAP Kinase Signaling System
(physiology)
- Male
- Pain
(chemically induced, metabolism)
- Pain Measurement
- Rats
- Rats, Sprague-Dawley
- Receptor, trkB
(genetics, metabolism)
- Sensory Receptor Cells
(cytology, drug effects, physiology)
- Substance P
(metabolism)
- TRPV Cation Channels
(genetics, metabolism)
- Tumor Necrosis Factor-alpha
(immunology, pharmacology)
- Up-Regulation
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