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Calcium entry via TRPV1 but not ASICs induces neuropeptide release from sensory neurons.
Mol Cell Neurosci. 2014 Jul; 61:13-22.MC

Abstract

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.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland.Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland.Department of Pharmacology and Toxicology, University of Lausanne, 1005 Lausanne, Switzerland. Electronic address: Stephan.Kellenberger@unil.ch.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24794232

Citation

Boillat, Aurélien, et al. "Calcium Entry Via TRPV1 but Not ASICs Induces Neuropeptide Release From Sensory Neurons." Molecular and Cellular Neurosciences, vol. 61, 2014, pp. 13-22.
Boillat A, Alijevic O, Kellenberger S. Calcium entry via TRPV1 but not ASICs induces neuropeptide release from sensory neurons. Mol Cell Neurosci. 2014;61:13-22.
Boillat, A., Alijevic, O., & Kellenberger, S. (2014). Calcium entry via TRPV1 but not ASICs induces neuropeptide release from sensory neurons. Molecular and Cellular Neurosciences, 61, 13-22. https://doi.org/10.1016/j.mcn.2014.04.007
Boillat A, Alijevic O, Kellenberger S. Calcium Entry Via TRPV1 but Not ASICs Induces Neuropeptide Release From Sensory Neurons. Mol Cell Neurosci. 2014;61:13-22. PubMed PMID: 24794232.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcium entry via TRPV1 but not ASICs induces neuropeptide release from sensory neurons. AU - Boillat,Aurélien, AU - Alijevic,Omar, AU - Kellenberger,Stephan, Y1 - 2014/04/30/ PY - 2013/10/08/received PY - 2014/03/14/revised PY - 2014/04/23/accepted PY - 2014/5/6/entrez PY - 2014/5/6/pubmed PY - 2015/4/16/medline KW - ASIC KW - Calcitonin gene-related peptide KW - Calcium KW - Proton KW - Sensory neuron KW - Substance P KW - TRPV1 SP - 13 EP - 22 JF - Molecular and cellular neurosciences JO - Mol Cell Neurosci VL - 61 N2 - 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. SN - 1095-9327 UR - https://www.unboundmedicine.com/medline/citation/24794232/Calcium_entry_via_TRPV1_but_not_ASICs_induces_neuropeptide_release_from_sensory_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1044-7431(14)00044-X DB - PRIME DP - Unbound Medicine ER -