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Mutations affecting glycinergic neurotransmission in hyperekplexia increase pain sensitivity

Vuilleumier, Pascal Henri ; Fritsche, Raphael ; Schliessbach, Jürg ; Schmitt, Bernhard ; Arendt-Nielsen, Lars ; Zeilhofer, Hanns Ulrich ; Curatolo, Michele

In: Brain, 2018, vol. 141, no. 1, p. 63-71

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    Titre
    • Mutations affecting glycinergic neurotransmission in hyperekplexia increase pain sensitivity
    Auteur
    • Vuilleumier, Pascal Henri. Department of Anaesthesiology and Pain Medicine, Bern University Hospital, University of Bern, Switzerland
    • Fritsche, Raphael. Department of Ophthalmology, Canton Hospital of Lucerne, Switzerland
    • Schliessbach, Jürg. Department of Anaesthesiology and Pain Medicine, Bern University Hospital, University of Bern, Switzerland
    • Schmitt, Bernhard. Department of Child Neurology, Children's Hospital, University of Zurich, Switzerland
    • Arendt-Nielsen, Lars. Center for Sensory-Motor Interaction, School of Medicine, University of Aalborg, Denmark
    • Zeilhofer, Hanns Ulrich. Institute of Pharmacology and Toxicology, University of Zurich, and Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology (ETH) Zurich, Switzerland
    • Curatolo, Michele. Center for Sensory-Motor Interaction, School of Medicine, University of Aalborg, Denmark
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Brain, 2018, vol. 141, no. 1, p. 63-71. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:331352
    Summary
    See Dickenson (doi:10.1093/brain/awx334) for a scientific commentary on this article. Hyperekplexia is a rare genetic disease resulting in glycine receptor dysfunction. Animal models implicate glycinergic and GABAergic inhibitory neurotransmission in spinal pain pathways. Vuilleumier et al. reveal lower pain thresholds in patients with hyperekplexia than in healthy controls, confirming the importance of glycinergic neurotransmission for central pain modulation in humans.