TRPA1 is a component of the nociceptive response to CO2

In humans, high concentrations of CO(2), as found in carbonated beverages, evoke a mixture of sensations that include a stinging or pungent quality. The stinging sensation is thought to originate with the activation of nociceptors, which innervate the respiratory, nasal, and oral epithelia. The mole...

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Bibliographic Details
Published in:The Journal of neuroscience 2010-09, Vol.30 (39), p.12958-12963
Main Authors: Wang, Yuanyuan Y, Chang, Rui B, Liman, Emily R
Format: Article
Language:English
Subjects:
Acrolein - analogs & derivatives
Acrolein - pharmacology
Animals
Brief Communications
Calcium Signaling - drug effects
Calcium Signaling - physiology
Carbon Dioxide - physiology
Cell Line
Humans
Hydrogen-Ion Concentration
Intracellular Fluid - drug effects
Intracellular Fluid - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Mouth - drug effects
Mouth - innervation
Nociceptors - drug effects
Nociceptors - physiology
Patch-Clamp Techniques - methods
Rats
Sensory Receptor Cells - drug effects
Sensory Receptor Cells - physiology
Transient Receptor Potential Channels - agonists
Transient Receptor Potential Channels - biosynthesis
Transient Receptor Potential Channels - physiology
Trigeminal Nerve - drug effects
Trigeminal Nerve - physiology
TRPA1 Cation Channel
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Summary:In humans, high concentrations of CO(2), as found in carbonated beverages, evoke a mixture of sensations that include a stinging or pungent quality. The stinging sensation is thought to originate with the activation of nociceptors, which innervate the respiratory, nasal, and oral epithelia. The molecular basis for this sensation is unknown. Here we show that CO(2) specifically activates a subpopulation of trigeminal neurons that express TRPA1, a mustard oil- and cinnamaldehyde-sensitive channel, and that these responses are dependent on a functional TRPA1 gene. TRPA1 is sufficient to mediate responses to CO(2) as TRPA1 channels expressed in HEK-293 cells, but not TRPV1 channels, were activated by bath-applied CO(2). CO(2) can diffuse into cells and produce intracellular acidification, which could gate TRPA1 channels. Consistent with this mechanism, TRPA1 channels in excised patches were activated in a dose-dependent manner by intracellular protons. We conclude that TRPA1, by sensing intracellular acidification, constitutes an important component of the nociceptive response to CO(2).
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.2715-10.2010