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François A, Schüetter N, Laffray S, et al. The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. Cell Rep. 2015;10(3):370-382doi: 10.1016/j.celrep.2014.12.042.
François, A., Schüetter, N., Laffray, S., Sanguesa, J., Pizzoccaro, A., Dubel, S., Mantilleri, A., Nargeot, J., Noël, J., Wood, J. N., Moqrich, A., Pongs, O., & Bourinet, E. (2015). The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. Cell reports, 10(3), 370-382. https://doi.org/10.1016/j.celrep.2014.12.042
François, Amaury, et al. "The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function." Cell reports vol. 10,3 (2015): 370-382. doi: https://doi.org/10.1016/j.celrep.2014.12.042
François A, Schüetter N, Laffray S, Sanguesa J, Pizzoccaro A, Dubel S, Mantilleri A, Nargeot J, Noël J, Wood JN, Moqrich A, Pongs O, Bourinet E. The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. Cell Rep. 2015 Jan 20;10(3):370-382. doi: 10.1016/j.celrep.2014.12.042. Epub 2015 Jan 15. PMID: 25600872.
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Cell Rep. 2015 Jan 20;10(3):370-382. doi: 10.1016/j.celrep.2014.12.042. Epub 2015 Jan 15.

The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function.

Cell reports

Amaury François, Niklas Schüetter, Sophie Laffray, Juan Sanguesa, Anne Pizzoccaro, Stefan Dubel, Annabelle Mantilleri, Joel Nargeot, Jacques Noël, John N Wood, Aziz Moqrich, Olaf Pongs, Emmanuel Bourinet

Affiliations

  1. Laboratories of Excellence, Ion Channel Science and Therapeutics, Institut de Génomique Fonctionnelle, 141 rue de la Cardonille, 34094 Montpellier, France; CNRS UMR5203, 34095 Montpellier, France; INSERM, U661, 34095 Montpellier, France; Université de Montpellier, 34095 Montpellier, France.
  2. Department of Physiology, University of Saarland, School of Medicine, Kirrberger Straße 1, 66424 Homburg, Germany.
  3. Aix-Marseille-Université, CNRS, Institut de Biologie du Développement de Marseille, UMR 7288, 13288 Marseille, France.
  4. Laboratories of Excellence, Ion Channel Science and Therapeutics, Institut de Génomique Fonctionnelle, 141 rue de la Cardonille, 34094 Montpellier, France; Université de Nice Sophia Antipolis, Institut de Pharmacologie Moléculaire et Cellulaire, UMR7275 CNRS, 660 route des lucioles, 06560 Valbonne, France.
  5. Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK.
  6. Laboratories of Excellence, Ion Channel Science and Therapeutics, Institut de Génomique Fonctionnelle, 141 rue de la Cardonille, 34094 Montpellier, France; CNRS UMR5203, 34095 Montpellier, France; INSERM, U661, 34095 Montpellier, France; Université de Montpellier, 34095 Montpellier, France. Electronic address: [email protected].

PMID: 25600872 DOI: 10.1016/j.celrep.2014.12.042

Abstract

The T-type calcium channel Cav3.2 emerges as a key regulator of sensory functions, but its expression pattern within primary afferent neurons and its contribution to modality-specific signaling remain obscure. Here, we elucidate this issue using a unique knockin/flox mouse strain wherein Cav3.2 is replaced by a functional Cav3.2-surface-ecliptic GFP fusion. We demonstrate that Cav3.2 is a selective marker of two major low-threshold mechanoreceptors (LTMRs), Aδ- and C-LTMRs, innervating the most abundant skin hair follicles. The presence of Cav3.2 along LTMR-fiber trajectories is consistent with critical roles at multiple sites, setting their strong excitability. Strikingly, the C-LTMR-specific knockout uncovers that Cav3.2 regulates light-touch perception and noxious mechanical cold and chemical sensations and is essential to build up that debilitates allodynic symptoms of neuropathic pain, a mechanism thought to be entirely A-LTMR specific. Collectively, our findings support a fundamental role for Cav3.2 in touch/pain pathophysiology, validating their critic pharmacological relevance to relieve mechanical and cold allodynia.

Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

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