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Persistent pain: the contribution of NaV1.9

Item Type:Editorial
Title:Persistent pain: the contribution of NaV1.9
Creators Name:Smith, E.S.J. and Momin, A.
Abstract:Sodium channels are crucial to the ability of sensory neurones to fire action potentials. Modulation of these ion channels can cause neurones to become sensitised leading to a state called hyperalgesia. A recent article by Ostman et al. demonstrates that the decreased inflammatory hyperalgesia observed in NaV1.9 knockout mice is due to the lack of upregulation of a persistent sodium current in sensory neurones by GTP-gamma-S. In neurones from wild type mice this upregulation causes a negative shift in sensory neurone threshold activation: sensitisation. This short article reviews the set of experiments that brought about this finding.
Keywords:Inflammation, Nociceptor, Sodium (Na+) channel, Animals, Mice
Source:Journal of Physiology
Page Range:2249-2250
Date:May 2008
Additional Information:The definitive version is available at www.blackwell-synergy.com
Official Publication:https://doi.org/10.1113/jphysiol.2008.152520
PubMed:View item in PubMed

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