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[Molecular mechanisms of nociception]
Makoto Tominaga1, Mitsuko Numazaki, Tohko Iida
1Department of Cellular and Molecular Physiology, Mie University School of Medicine, 2-174, Edobashi, Tsu, 514-8507 Japan.
Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology
|July 30, 2003
Summary
Capsaicin activates the TRPV1 receptor, causing burning pain. Tissue damage releases chemicals that lower TRPV1
Area of Science:
- Molecular biology
- Neuroscience
- Pain research
Background:
- Capsaicin activates nociceptors via the TRPV1 receptor.
- TRPV1 channels are activated by heat, protons, and capsaicin.
- TRPV1 is crucial for pain sensation and thermal hyperalgesia.
Purpose of the Study:
- Investigate the role of ATP and bradykinin in TRPV1 activation.
- Determine the mechanism by which tissue damage mediators sensitize TRPV1.
- Identify novel pathways for pain sensation.
Main Methods:
- Functional expression of TRPV1 in cells.
- Electrophysiological recordings of TRPV1 currents.
- Analysis of TRPV1 phosphorylation by PKC epsilon.
Main Results:
- ATP and bradykinin sensitize TRPV1 channels.
- These mediators reduce the temperature threshold for TRPV1 activation.
- PKC epsilon directly phosphorylates TRPV1 at specific serine residues.
Conclusions:
- ATP and bradykinin, released during tissue damage, can trigger pain by sensitizing TRPV1.
- This sensitization lowers the activation temperature, causing pain at normal body temperatures.
- TRPV1 phosphorylation by PKC epsilon is a key mechanism in this process.