1. Department of Cellular and Molecular Pharmacology University of California, San Francisco, California 94143-2140, USA
2. Department of Neurology, University of California, San Francisco, California 94143-2140, USA
3. Department of Clinical Pharmacology, Institute of Laboratory Medicine, Lund University Hospital, SE-221 85 Lund, Sweden
4. Present address: Department of Physiology, College of Osteopathic Medicine, University of New England, 11 Hills Beach Road, Biddeford, Maine 04005, USA

Correspondence to: David Julius¹ Email: julius@cmp.ucsf.edu

Abstract

Wasabi, horseradish and mustard owe their pungency to isothiocyanate compounds. Topical application of mustard oil (allyl isothiocyanate) to the skin activates underlying sensory nerve endings, thereby producing pain, inflammation and robust hypersensitivity to thermal and mechanical stimuli^{1, 2}. Despite their widespread use in both the kitchen and the laboratory, the molecular mechanism through which isothiocyanates mediate their effects remains unknown. Here we show that mustard oil depolarizes a subpopulation of primary sensory neurons that are also activated by capsaicin, the pungent ingredient in chilli peppers, and by ⁹-tetrahydrocannabinol (THC), the psychoactive component of marijuana. Both allyl isothiocyanate and THC mediate their excitatory effects by activating ANKTM1, a member of the TRP ion channel family recently implicated in the detection of noxious cold^{3, 4}. These findings identify a cellular and molecular target for the pungent action of mustard oils and support an emerging role for TRP channels as ionotropic cannabinoid receptors^{5, 6, 7, 8}.

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