The Cell and Molecular Basis of Mechanical, Cold, and Inflammatory Pain
Top Cited Papers
- 1 August 2008
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 321 (5889), 702-705
- https://doi.org/10.1126/science.1156916
Abstract
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 Nav1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing.Keywords
This publication has 24 references indexed in Scilit:
- TRPV1 Unlike TRPV2 Is Restricted to a Subset of Mechanically Insensitive Cutaneous Nociceptors Responding to HeatThe Journal of Pain, 2008
- TRPA1 mediates formalin-induced painProceedings of the National Academy of Sciences of the United States of America, 2007
- Sensory neuron sodium channel Nav1.8 is essential for pain at low temperaturesNature, 2007
- The menthol receptor TRPM8 is the principal detector of environmental coldNature, 2007
- Ideas about pain, a historical viewNature Reviews Neuroscience, 2007
- Transient receptor potential ion channels as participants in thermosensation and thermoregulationAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2007
- The Voltage-Gated Sodium Channel Nav1.9 Is an Effector of Peripheral Inflammatory Pain HypersensitivityJournal of Neuroscience, 2006
- μO-conotoxin MrVIB selectively blocks Na v 1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficitsProceedings of the National Academy of Sciences of the United States of America, 2006
- Nociceptor-derived brain-derived neurotrophic factor regulates acute and inflammatory but not neuropathic painMolecular and Cellular Neuroscience, 2006
- Phenotype and Function of Somatic Primary Afferent Nociceptive Neurones with C‐, Aδ‐ or Aα/β‐FibresExperimental Physiology, 2002