TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide-Reference-Cited by-同舟云学术

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TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

Published:2017-07-06 Issue:1 Volume:12 Page:
ISSN:1750-1326
Container-title:Molecular Neurodegeneration
language:en
Short-container-title:Mol Neurodegeneration

Author:

Bosson Anthony,Paumier Adrien,Boisseau Sylvie,Jacquier-Sarlin Muriel,Buisson Alain,Albrieux Mireille^ORCID

Funder

Institut National de la Santé et de la Recherche Médicale

Université Grenoble Alpes

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Neurology (clinical),Molecular Biology

Link

http://link.springer.com/content/pdf/10.1186/s13024-017-0194-8.pdf

Reference51 articles.

1. Haass C, Selkoe DJ. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat Rev Mol Cell Biol. 2007;8:101–12.

2. Verkhratsky A, Steinhauser C. Ion channels in glial cells. Brain Res Brain Res Rev. 2000;32:380–412.

3. Panatier A, Theodosis DT, Mothet JP, Touquet B, Pollegioni L, Poulain DA, et al. Glia-derived D-serine controls NMDA receptor activity and synaptic memory. Cell. 2006;125:775–84.

4. Haydon PG. GLIA: listening and talking to the synapse. Nat Rev Neurosci. 2001;2:185–93.

5. Araque A, Parpura V, Sanzgiri RP, Haydon PG. Tripartite synapses: glia, the unacknowledged partner. Trends Neurosci. 1999;22:208–15.

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