NaV1.9: a sodium channel linked to human pain

doi:10.1038/nrn3977

Review

. 2015 Sep;16(9):511-9.

doi: 10.1038/nrn3977. Epub 2015 Aug 5.

NaV1.9: a sodium channel linked to human pain

Sulayman D Dib-Hajj¹, Joel A Black¹, Stephen G Waxman¹

Affiliations

Affiliation

¹ Department of Neurology and the Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA; and the Rehabilitation Research Center at the Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut 06516, USA.

PMID: 26243570
DOI: 10.1038/nrn3977

Review

NaV1.9: a sodium channel linked to human pain

Sulayman D Dib-Hajj et al. Nat Rev Neurosci. 2015 Sep.

. 2015 Sep;16(9):511-9.

doi: 10.1038/nrn3977. Epub 2015 Aug 5.

Authors

Sulayman D Dib-Hajj¹, Joel A Black¹, Stephen G Waxman¹

Affiliation

¹ Department of Neurology and the Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510, USA; and the Rehabilitation Research Center at the Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut 06516, USA.

PMID: 26243570
DOI: 10.1038/nrn3977

Abstract

The voltage-gated sodium channel Na(V)1.9 is preferentially expressed in nociceptors and has been shown in rodent models to have a major role in inflammatory and neuropathic pain. These studies suggest that by selectively targeting Na(V)1.9, it might be possible to ameliorate pain without inducing adverse CNS side effects such as sedation, confusion and addictive potential. Three recent studies in humans--two genetic and functional studies in rare genetic disorders, and a third study showing a role for Na(V)1.9 in painful peripheral neuropathy--have demonstrated that Na(V)1.9 plays an important part both in regulating sensory neuron excitability and in pain signalling. With this human validation, attention is turning to this channel as a potential therapeutic target for pain.

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References

1. J Neurosci. 2006 Jul 5;26(27):7281-92 - PubMed
1. Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9382-7 - PubMed
1. J Neurophysiol. 2014 Apr;111(7):1429-43 - PubMed
1. J Neurosci. 2013 Aug 28;33(35):14087-97 - PubMed
1. Mol Ther. 2014 Aug;22(8):1530-43 - PubMed

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[1] J Neurosci. 2006 Jul 5;26(27):7281-92 - PubMed

[2] J Neurosci. 2006 Jul 5;26(27):7281-92 - PubMed

[3] Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9382-7 - PubMed

[4] Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9382-7 - PubMed

[5] J Neurophysiol. 2014 Apr;111(7):1429-43 - PubMed

[6] J Neurophysiol. 2014 Apr;111(7):1429-43 - PubMed

[7] J Neurosci. 2013 Aug 28;33(35):14087-97 - PubMed

[8] J Neurosci. 2013 Aug 28;33(35):14087-97 - PubMed

[9] Mol Ther. 2014 Aug;22(8):1530-43 - PubMed

[10] Mol Ther. 2014 Aug;22(8):1530-43 - PubMed

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NaV1.9: a sodium channel linked to human pain

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NaV1.9: a sodium channel linked to human pain

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