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

Citation
Bj. Kerr et al., A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain, NEUROREPORT, 12(14), 2001, pp. 3077-3080
Citations number
26
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROREPORT
ISSN journal
09594965 → ACNP
Volume
12
Issue
14
Year of publication
2001
Pages
3077 - 3080
Database
ISI
SICI code
0959-4965(20011008)12:14<3077:ARFTTS>2.0.ZU;2-D
Abstract
The tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 is expresse d only in nociceptive sensory neurons. This channel has been proposed to co ntribute significantly to the sensitization of primary sensory neurons afte r injury. We have studied the nociceptive behaviours of mice carrying a nul l mutation in the Nav 1.8 gene (Nav 1.8 -/-) in models of peripheral inflam mation 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 PGE(2)-evoked hypersensitivity. Neur opathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds follow ing peripheral nerve injury. NeuroReport 12:3077-3080 (C) 2001 Lippincott W illiams & Wilkins.