The cell and molecular basis of mechanical, cold, and inflammatory pain |
| |
| Authors: | 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 |
| |
| Institution: | Molecular Nociception Group, University College London (UCL), Gower Street, London, WC1E 6BT, UK. |
| |
| 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 Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing. |
| |
| Keywords: | |
| 本文献已被 PubMed 等数据库收录！ |
|
