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TRPV1 is activated by both acidic and basic pH

Academic Article
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Overview

authors

  • Dhaka, A.
  • Uzzell, V.
  • Dubin, Adrienne
  • Mathur, J.
  • Petrus, M.
  • Bandell, M.
  • Patapoutian, Ardem

publication date

  • January 2009

journal

  • Journal of Neuroscience  Journal

abstract

  • 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.

subject areas

  • Acids
  • Ammonium Chloride
  • Animals
  • Calcium
  • Capsaicin
  • Cell Line, Transformed
  • Ganglia, Spinal
  • Humans
  • Hydrogen-Ion Concentration
  • Luminescent Proteins
  • Membrane Potentials
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Models, Biological
  • Mutagenesis, Site-Directed
  • Patch-Clamp Techniques
  • Pyrazines
  • Pyridines
  • Sensory Receptor Cells
  • Sensory System Agents
  • TRPV Cation Channels
  • Transfection
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Research

keywords

  • TRPA1
  • TRPV1
  • alkalization
  • ammonia
  • nociception
  • pH
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Identity

PubMed Central ID

  • PMC2729567

International Standard Serial Number (ISSN)

  • 0270-6474

Digital Object Identifier (DOI)

  • 10.1523/jneurosci.4901-08.2009

PubMed ID

  • 19129393
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Additional Document Info

start page

  • 153

end page

  • 158

volume

  • 29

issue

  • 1

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