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Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain.

We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium cur... Full description

Journal Title: PloS one 2014, Vol.9(12), p.e114623
Main Author: Liu, Xiao-Dan
Other Authors: Yang, Jing-Jing , Fang, Dong , Cai, Jie , Wan, You , Xing, Guo-Gang
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0114623
Link: http://search.proquest.com/docview/1639497653/?pq-origsite=primo
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title: Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain.
format: Article
creator:
  • Liu, Xiao-Dan
  • Yang, Jing-Jing
  • Fang, Dong
  • Cai, Jie
  • Wan, You
  • Xing, Guo-Gang
subjects:
  • Aniline Compounds–Pharmacology
  • Animals–Therapeutic Use
  • Bone Neoplasms–Complications
  • Cell Line, Tumor–Drug Effects
  • Cell Membrane–Metabolism
  • Electrophysiological Phenomena–Drug Effects
  • Female–Pharmacology
  • Furans–Therapeutic Use
  • Ganglia, Spinal–Drug Effects
  • Gene Expression Regulation, Neoplastic–Pathology
  • Hyperalgesia–Drug Effects
  • Nav1.8 Voltage-Gated Sodium Channel–Drug Therapy
  • Neurons–Etiology
  • Pain–Metabolism
  • Rats–Drug Effects
  • Rats, Sprague-Dawley–Pathology
  • Sodium Channel Blockers–Drug Therapy
  • Up-Regulation–Etiology
  • Up-Regulation–Metabolism
  • Up-Regulation–Pathology
  • Up-Regulation–Pharmacology
  • Up-Regulation–Therapeutic Use
  • Up-Regulation–Drug Effects
  • A 803467
  • Aniline Compounds
  • Furans
  • Nav1.8 Voltage-Gated Sodium Channel
  • Scn10a Protein, Rat
  • Sodium Channel Blockers
ispartof: PloS one, 2014, Vol.9(12), p.e114623
description: We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. We speculate that the Nav1.8 sodium channel is a potential candidate responsible for the enhanced excitability of DRG neurons in rats with bone cancer pain. Here, using electrophysiology, Western blot and behavior assays, we documented that the current density of TTX-R sodium channels, especially the Nav1.8 channel, increased significantly in DRG neurons of rats with cancer-induced bone pain. This increase may be due to an increased expression of Nav1.8 on the membrane of DRG neurons. Accordantly, blockade of Nav1.8 sodium channels by its selective blocker A-803467 significantly alleviated the cancer-induced mechanical allodynia and thermal hyperalgesia in rats. Taken together, these results suggest that functional upregulation of Nav1.8 channels on the membrane of DRG neurons contributes to the development of cancer-induced bone pain.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0114623
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleFunctional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain.
creatorLiu, Xiao-Dan ; Yang, Jing-Jing ; Fang, Dong ; Cai, Jie ; Wan, You ; Xing, Guo-Gang
contributorLiu, Xiao-Dan (correspondence author) ; Liu, Xiao-Dan (record owner)
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0114623
subjectAniline Compounds–Pharmacology ; Animals–Therapeutic Use ; Bone Neoplasms–Complications ; Cell Line, Tumor–Drug Effects ; Cell Membrane–Metabolism ; Electrophysiological Phenomena–Drug Effects ; Female–Pharmacology ; Furans–Therapeutic Use ; Ganglia, Spinal–Drug Effects ; Gene Expression Regulation, Neoplastic–Pathology ; Hyperalgesia–Drug Effects ; Nav1.8 Voltage-Gated Sodium Channel–Drug Therapy ; Neurons–Etiology ; Pain–Metabolism ; Rats–Drug Effects ; Rats, Sprague-Dawley–Pathology ; Sodium Channel Blockers–Drug Therapy ; Up-Regulation–Etiology ; Up-Regulation–Metabolism ; Up-Regulation–Pathology ; Up-Regulation–Pharmacology ; Up-Regulation–Therapeutic Use ; Up-Regulation–Drug Effects ; A 803467 ; Aniline Compounds ; Furans ; Nav1.8 Voltage-Gated Sodium Channel ; Scn10a Protein, Rat ; Sodium Channel Blockers
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descriptionWe have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. We speculate that the Nav1.8 sodium channel is a potential candidate responsible for the enhanced excitability of DRG neurons in rats with bone cancer pain. Here, using electrophysiology, Western blot and behavior assays, we documented that the current density of TTX-R sodium channels, especially the Nav1.8 channel, increased significantly in DRG neurons of rats with cancer-induced bone pain. This increase may be due to an increased expression of Nav1.8 on the membrane of DRG neurons. Accordantly, blockade of Nav1.8 sodium channels by its selective blocker A-803467 significantly alleviated the cancer-induced mechanical allodynia and thermal hyperalgesia in rats. Taken together, these results suggest that functional upregulation of Nav1.8 channels on the membrane of DRG neurons contributes to the development of cancer-induced bone pain.
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titleFunctional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain.
authorLiu, Xiao-Dan ; Yang, Jing-Jing ; Fang, Dong ; Cai, Jie ; Wan, You ; Xing, Guo-Gang
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