Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain - PubMed (original) (raw)
Comparative Study
. 2004 Apr;108(3):237-247.
doi: 10.1016/j.pain.2003.12.035.
Affiliations
- PMID: 15030943
- DOI: 10.1016/j.pain.2003.12.035
Comparative Study
Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain
Joel A Black et al. Pain. 2004 Apr.
Abstract
Nociceptive neurons within dorsal root ganglia (DRG) express multiple voltage-gated sodium channels, of which the tetrodotoxin-resistant (TTX-R) channel Na(v)1.8 has been suggested to play a major role in inflammatory pain. Previous work has shown that acute administration of inflammatory mediators, including prostaglandin E2 (PGE2), serotonin, and adenosine, modulates TTX-R current in DRG neurons, producing increased current amplitude and a hyperpolarizing shift of its activation curve. In addition, 4 days following injection of carrageenan into the hind paw, an established model of inflammatory pain, Na(v)1.8 mRNA and slowly-inactivating TTX-R current are increased in DRG neurons projecting to the affected paw. In the present study, the expression of sodium channels Na(v)1.1-Na(v)1.9 in small (< or = 25 micromdiameter) DRG neurons was examined with in situ hybridization, immunocytochemistry, Western blot and whole-cell patch-clamp methods following carrageenan injection into the peripheral projection fields of these cells. The results demonstrate that, following carrageenan injection, there is increased expression of TTX-S channels Na(v)1.3 and Na(v)1.7 and a parallel increase in TTX-S currents. The previously reported upregulation of Na(v)1.8 and slowly-inactivating TTX-R current is not accompanied by upregulation of mRNA or protein for Na(v)1.9, an additional TTX-R channel that is expressed in some DRG neurons. These observations demonstrate that chronic inflammation results in an upregulation in the expression of both TTX-S and TTX-R sodium channels, and suggest that TTX-S sodium channels may also contribute, at least in part, to pain associated with inflammation.
Similar articles
- SNS Na+ channel expression increases in dorsal root ganglion neurons in the carrageenan inflammatory pain model.
Tanaka M, Cummins TR, Ishikawa K, Dib-Hajj SD, Black JA, Waxman SG. Tanaka M, et al. Neuroreport. 1998 Apr 20;9(6):967-72. doi: 10.1097/00001756-199804200-00003. Neuroreport. 1998. PMID: 9601651 - Functional tetrodotoxin-resistant Na(+) channels are expressed presynaptically in rat dorsal root ganglia neurons.
Medvedeva YV, Kim MS, Schnizler K, Usachev YM. Medvedeva YV, et al. Neuroscience. 2009 Mar 17;159(2):559-69. doi: 10.1016/j.neuroscience.2008.12.029. Epub 2008 Dec 30. Neuroscience. 2009. PMID: 19162133 - Early painful diabetic neuropathy is associated with differential changes in tetrodotoxin-sensitive and -resistant sodium channels in dorsal root ganglion neurons in the rat.
Hong S, Morrow TJ, Paulson PE, Isom LL, Wiley JW. Hong S, et al. J Biol Chem. 2004 Jul 9;279(28):29341-50. doi: 10.1074/jbc.M404167200. Epub 2004 May 3. J Biol Chem. 2004. PMID: 15123645 Free PMC article. - Modulation of sodium channels in primary afferent neurons.
Bevan S, Storey N. Bevan S, et al. Novartis Found Symp. 2002;241:144-53; discussion 153-8, 226-32. Novartis Found Symp. 2002. PMID: 11771643 Review. - Tetrodotoxin-resistant sodium channels.
Yoshida S. Yoshida S. Cell Mol Neurobiol. 1994 Jun;14(3):227-44. doi: 10.1007/BF02088322. Cell Mol Neurobiol. 1994. PMID: 7712513 Review.
Cited by
- Electrophysiological correlates of hyperalgesic priming in vitro and in vivo.
Hendrich J, Alvarez P, Joseph EK, Chen X, Bogen O, Levine JD. Hendrich J, et al. Pain. 2013 Oct;154(10):2207-2215. doi: 10.1016/j.pain.2013.07.004. Epub 2013 Jul 4. Pain. 2013. PMID: 23831864 Free PMC article. - Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia.
Huang CP, Chen HN, Su HL, Hsieh CL, Chen WH, Lai ZR, Lin YW. Huang CP, et al. Evid Based Complement Alternat Med. 2013;2013:312184. doi: 10.1155/2013/312184. Epub 2013 Mar 19. Evid Based Complement Alternat Med. 2013. PMID: 23573123 Free PMC article. - Voltage-gated sodium channels in diabetic sensory neuropathy: Function, modulation, and therapeutic potential.
Bigsby S, Neapetung J, Campanucci VA. Bigsby S, et al. Front Cell Neurosci. 2022 Nov 17;16:994585. doi: 10.3389/fncel.2022.994585. eCollection 2022. Front Cell Neurosci. 2022. PMID: 36467605 Free PMC article. Review. - Understanding inflammatory pain: ion channels contributing to acute and chronic nociception.
Linley JE, Rose K, Ooi L, Gamper N. Linley JE, et al. Pflugers Arch. 2010 Apr;459(5):657-69. doi: 10.1007/s00424-010-0784-6. Epub 2010 Feb 17. Pflugers Arch. 2010. PMID: 20162302 Review. - Temporal coding by cochlear nucleus bushy cells in DBA/2J mice with early onset hearing loss.
Wang Y, Manis PB. Wang Y, et al. J Assoc Res Otolaryngol. 2006 Dec;7(4):412-24. doi: 10.1007/s10162-006-0052-9. Epub 2006 Oct 26. J Assoc Res Otolaryngol. 2006. PMID: 17066341 Free PMC article.
References
- Akopian AN, Sivilotti L, Wood JN. A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons. Nature. 1996;379:258-262.
- Akopian AN, Souslova V, England S, Okuse K, Ogata N, Ure J, Smith A, Kerr BJ, McMahon SB, Boyce S, Hill R, Stanfa LC, Dickenson AH, Wood JN. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci. 1999;2:541-548.
- Baker MD, Wood JN. Involvement of Na+ channels in pain pathways. Trends Pharmacol Sci. 2001;22:27-31.
- Baker MD, Chandra SY, Ding Y, Waxman SG, Wood JN. GTP-induced tetrotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones. J Physiol. 2003;548:373-382.
- Black JA, Dib-Hajj S, McNabola K, Jeste S, Rizzo MA, Kocsis JD, Waxman SG. Spinal sensory neurons express multiple sodium channel α-subunit mRNAs. Brain Res. 1996;43:117-131.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical