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The Journal of Neuroscience, January 7, 2009, 29(1):153-158; doi:10.1523/JNEUROSCI.4901-08.2009

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Brief Communications
TRPV1 Is Activated by Both Acidic and Basic pH

Ajay Dhaka,1 * Valerie Uzzell,1 * Adrienne E. Dubin,1 Jayanti Mathur,2 Matt Petrus,2 Michael Bandell,2 and Ardem Patapoutian1,2

1Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, and 2Genomics Institute of the Novartis Research Foundation, San Diego, California 92121

Correspondence should be addressed to Prof. Ardem Patapoutian, Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, ICND210F, La Jolla, CA 92037. Email: apatapou{at}gnf.org

Maintaining physiological pH is required for survival, and exposure to alkaline chemicals such as ammonia (smelling salts) elicits severe pain and inflammation through unknown mechanisms. TRPV1, the capsaicin receptor, is an integrator of noxious stimuli including heat and extracellular acidic pH. Here, we report that ammonia activates TRPV1, TRPA1 (another polymodal nocisensor), and other unknown receptor(s) expressed in sensory neurons. Ammonia and intracellular alkalization activate TRPV1 through a mechanism that involves a cytoplasmic histidine residue, not used by other TRPV1 agonists such as heat, capsaicin or low pH. Our studies show that TRPV1 detects both acidic and basic deviations from homeostatic pH.

Key words: TRPA1; TRPV1; ammonia; nociception; alkalization; pH

Received Oct. 10, 2008; accepted Nov. 11, 2008.

Correspondence should be addressed to Prof. Ardem Patapoutian, Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, ICND210F, La Jolla, CA 92037. Email: apatapou{at}gnf.org




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