The cloned capsaicin receptor integrates multiple pain-producing stimuli

Makoto Tominaga, Michael J. Caterina, Annika B. Malmberg, Tobias A. Rosen, Heather Gilbert, Kate Skinner, Brigitte E. Raumann, Allan I. Basbaum, David Julius

Research output: Contribution to journalArticlepeer-review

Abstract

Capsaicin, the main pungent ingredient in 'hot' chili peppers, elicits burning pain by activating specific (vanilloid) receptors on sensory nerve endings. The cloned vanilloid receptor (VR1) is a cation channel that is also activated by noxious heat. Here, analysis of heat-evoked single channel currents in excised membrane patches suggests that heat gates VR1 directly. We also show that protons decrease the temperature threshold for VR1 activation such that even moderately acidic conditions (pH ≤ 5.9) activate VR1 at room temperature. VR1 can therefore be viewed as a molecular integrator of chemical and physical stimuli that elicit pain. Immunocytochemical analysis indicates that the receptor is located in a neurochemically heterogeneous population of small diameter primary afferent fibers. A role for VR1 in injury-induced hypersensitivity at the level of the sensory neuron is presented.

Original languageEnglish (US)
Pages (from-to)531-543
Number of pages13
JournalNeuron
Volume21
Issue number3
DOIs
StatePublished - Sep 1998
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

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