Literature DB >> 11568640

A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain.

B J Kerr1, V Souslova, S B McMahon, J N Wood.   

Abstract

The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expressed only in nociceptive sensory neurons. This channel has been proposed to contribute significantly to the sensitization of primary sensory neurons after injury. We have studied the nociceptive behaviours of mice carrying a null mutation in the Nav 1.8 gene (Nav 1.8 -/-) in models of peripheral inflammation as well as a model of neuropathic pain. The results from the present studies reveal that Nav 1.8 is a necessary mediator of NGF-induced thermal hyperalgesia but is not essential for PGE2-evoked hypersensitivity. Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury.

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Year:  2001        PMID： 11568640     DOI： 10.1097/00001756-200110080-00019

Source DB:  PubMed          Journal:  Neuroreport        ISSN： 0959-4965            Impact factor:   1.837


  72 in total

1.  The majority of myelinated and unmyelinated sensory nerve fibers that innervate bone express the tropomyosin receptor kinase A.

Authors:  G Castañeda-Corral; J M Jimenez-Andrade; A P Bloom; R N Taylor; W G Mantyh; M J Kaczmarska; J R Ghilardi; P W Mantyh
Journal:  Neuroscience       Date:  2011-01-26       Impact factor: 3.590

2.  The tetrodotoxin-resistant Na+ channel Nav1.8 is essential for the expression of spontaneous activity in damaged sensory axons of mice.

Authors:  Carolina Roza; Jennifer M A Laird; Veronika Souslova; John N Wood; Fernando Cervero
Journal:  J Physiol       Date:  2003-06-24       Impact factor: 5.182

Review 3.  Strategies for finding new pharmacological targets for neuropathic pain.

Authors:  Marshal Devor
Journal:  Curr Pain Headache Rep       Date:  2004-06

Review 4.  Putative therapeutic targets in the treatment of visceral hyperalgesia.

Authors:  S Collins
Journal:  Gut       Date:  2004-03       Impact factor: 23.059

5.  PKA-induced internalization of slack KNa channels produces dorsal root ganglion neuron hyperexcitability.

Authors:  Megan O Nuwer; Kelly E Picchione; Arin Bhattacharjee
Journal:  J Neurosci       Date:  2010-10-20       Impact factor: 6.167

6.  Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.

Authors:  Birgit T Priest; Beth A Murphy; Jill A Lindia; Carmen Diaz; Catherine Abbadie; Amy M Ritter; Paul Liberator; Leslie M Iyer; Shera F Kash; Martin G Kohler; Gregory J Kaczorowski; D Euan MacIntyre; William J Martin
Journal:  Proc Natl Acad Sci U S A       Date:  2005-06-17       Impact factor: 11.205

7.  Subtype-selective sodium channel blockers promise a new era of pain research.

Authors:  Birgit T Priest; Gregory J Kaczorowski
Journal:  Proc Natl Acad Sci U S A       Date:  2007-05-08       Impact factor: 11.205

Review 8.  Peripheral nerve injury modulates neurotrophin signaling in the peripheral and central nervous system.

Authors:  Mette Richner; Maj Ulrichsen; Siri Lander Elmegaard; Ruthe Dieu; Lone Tjener Pallesen; Christian Bjerggaard Vaegter
Journal:  Mol Neurobiol       Date:  2014-04-22       Impact factor: 5.590

9.  Structural determinants of drugs acting on the Nav1.8 channel.

Authors:  Liam E Browne; Frank E Blaney; Shahnaz P Yusaf; Jeff J Clare; Dennis Wray
Journal:  J Biol Chem       Date:  2009-02-19       Impact factor: 5.157

10.  Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathy.

Authors:  Devang Kashyap Thakor; Audrey Lin; Yoshizo Matsuka; Edward M Meyer; Supanigar Ruangsri; Ichiro Nishimura; Igor Spigelman
Journal:  Mol Pain       Date:  2009-03-25       Impact factor: 3.395
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