Publication Date:
2008-08-02
Description:
Peripheral pain pathways are activated by a range of stimuli. We used diphtheria toxin to kill all mouse postmitotic sensory neurons expressing the sodium channel Nav1.8. Mice showed normal motor activity and low-threshold mechanical and acute noxious heat responses but did not respond to noxious mechanical pressure or cold. They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammatory insults. In contrast, nerve injury led to heightened pain sensitivity to thermal and mechanical stimuli indistinguishable from that seen with normal littermates. Pain behavior correlates well with central input from sensory neurons measured electrophysiologically in vivo. These data demonstrate that Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abrahamsen, Bjarke -- Zhao, Jing -- Asante, Curtis O -- Cendan, Cruz Miguel -- Marsh, Steve -- Martinez-Barbera, Juan Pedro -- Nassar, Mohammed A -- Dickenson, Anthony H -- Wood, John N -- BB/F000227/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G9717869/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):702-5. doi: 10.1126/science.1156916.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Nociception Group, University College London (UCL), Gower Street, London, WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669863" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Cold Temperature
;
Electrophysiology
;
Freund's Adjuvant
;
Hot Temperature
;
Inflammation/*physiopathology
;
Mice
;
Mice, Knockout
;
NAV1.8 Voltage-Gated Sodium Channel
;
Neurons, Afferent/*physiology
;
Nociceptors/physiology
;
Pain/*physiopathology
;
Pain Measurement
;
Pain Threshold
;
Pressure
;
Sodium Channels/genetics/*metabolism
;
TRPV Cation Channels/genetics/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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