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Calcium entry via TRPV1 but not ASICs induces neuropeptide release from sensory neurons.

  • Boillat A Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland.
  • Alijevic O Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland.
  • Kellenberger S Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland. Electronic address: Stephan.Kellenberger@unil.ch.
  • 2014-05-06
Published in:
  • Molecular and cellular neurosciences. - 2014
ASIC
Calcitonin gene-related peptide
Calcium
Proton
Sensory neuron
Substance P
TRPV1
Acid Sensing Ion Channel Blockers
Acid Sensing Ion Channels
Acids
Amiloride
Animals
Calcitonin Gene-Related Peptide
Calcium
Calcium Channel Blockers
Cell Count
Cells, Cultured
GABA Antagonists
Ganglia, Spinal
Hydrogen-Ion Concentration
Phosphopyruvate Hydratase
Picrotoxin
Pyrazines
Pyridines
Rats
Sensory Receptor Cells
Substance P
TRPV Cation Channels
English Inflammatory mediators induce neuropeptide release from nociceptive nerve endings and cell bodies, causing increased local blood flow and vascular leakage resulting in edema. Neuropeptide release from sensory neurons depends on an increase in intracellular Ca(2+) concentration. In this study we investigated the role of two types of pH sensors in acid-induced Ca(2+) entry and neuropeptide release from dorsal root ganglion (DRG) neurons. The transient receptor potential vanilloid 1 channel (TRPV1) and acid-sensing ion channels (ASICs) are both H(+)-activated ion channels present in these neurons, and are therefore potential pH sensors for this process. We demonstrate with in situ hybridization and immunocytochemistry that TRPV1 and several ASIC subunits are co-expressed with neuropeptides in DRG neurons. The activation of ASICs and of TRPV1 led to an increase in intracellular Ca(2+) concentration. While TRPV1 has a high Ca(2+) permeability and allows direct Ca(2+) entry when activated, we show here that ASICs of DRG neurons mediate Ca(2+) entry mostly by depolarization-induced activation of voltage-gated Ca(2+) channels and only to a small extent via the pore of Ca(2+)-permeable ASICs. Extracellular acidification led to the release of the neuropeptide calcitonin gene-related peptide from DRG neurons. The pH dependence and the pharmacological profile indicated that TRPV1, but not ASICs, induced neuropeptide secretion. In conclusion, this study shows that although both TRPV1 and ASICs mediate Ca(2+) influx, TRPV1 is the principal sensor for acid-induced neuropeptide secretion from sensory neurons.
Language
  • English
Open access status
green
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Persistent URL
https://roar.hep-bejune.ch/global/documents/148086
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