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Behavioural alterations and morphological changes are attenuated by the lack of TRPA1 receptors in the cuprizone-induced demyelination model in mice

  • Published:2018-07 Issue: Volume:320 Page:1-10
  • ISSN:0165-5728
  • Container-title:Journal of Neuroimmunology
  • language:en
  • Short-container-title:Journal of Neuroimmunology

Author:

Bölcskei Kata,Kriszta Gábor,Sághy Éva,Payrits Maja,Sipos Éva,Vranesics Anett,Berente Zoltán,Ábrahám Hajnalka,Ács Péter,Komoly Sámuel,Pintér Erika

Funder

Hungarian grant National Brain Research Program-A

National Excellence Program

Ministry of Human Capacities

Publisher

Elsevier BV

Subject

Clinical Neurology,Neurology,Immunology,Immunology and Allergy

Reference39 articles.

1. Pathogenesis of Multiple Sclerosis: What Can We Learn from the Cuprizone Model;Ács,2012

2. TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide;Bosson;Mol. Neurodegener.,2017

3. Reduced astrocytic NF-κB activation by laquinimod protects from cuprizone-induced demyelination;Brück;Acta Neuropathol. (Berl.),2012

4. TRPA1 as a drug target—promise and challenges;Chen;Naunyn Schmiedeberg's Arch. Pharmacol.,2015

5. The functions of TRPA1 and TRPV1: moving away from sensory nerves;Fernandes;Br. J. Pharmacol.,2012
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