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Neural Plasticity
Volume 2016 (2016), Article ID 1680905, 7 pages
Review Article

Glia and TRPM2 Channels in Plasticity of Central Nervous System and Alzheimer’s Diseases

1Key Laboratory of Orthopedics of Gansu Province, The Second Hospital of Lanzhou University, No. 82 Cui Ying Men, Lanzhou, Gansu 730030, China
2Department of Pharmacology & Therapeutics, University of Manitoba, Canada
3Kleysen Institute for Advanced Medicine, University of Manitoba, 710 William Avenue, SR426 Winnipeg, MB, Canada R3E 0Z3
4Leslie Dan Faculty of Pharmacy, University of Toronto, 144 College Street, Toronto, ON, Canada M5S 3M2

Received 11 October 2015; Revised 25 December 2015; Accepted 29 December 2015

Academic Editor: Jason H. Huang

Copyright © 2016 Jing Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Synaptic plasticity refers to the ability of neurons to strengthen or weaken synaptic efficacy in response to activity and is the basis for learning and memory. Glial cells communicate with neurons and in this way contribute in part to plasticity in the CNS and to the pathology of Alzheimer’s disease (AD), a neurodegenerative disease in which impaired synaptic plasticity is causally implicated. The transient receptor potential melastatin member 2 (TRPM2) channel is a nonselective Ca2+-permeable channel expressed in both glial cells (microglia and astrocytes) and neurons. Recent studies indicated that TRPM2 regulates synaptic plasticity as well as the activation of glial cells. TRPM2 also modulates oxidative stress and inflammation through interaction with glial cells. As both oxidative stress and inflammation have been implicated in AD pathology, this suggests a possible contribution of TRPM2 to disease processes. Through modulating the homeostasis of glutathione, TRPM2 is involved in the process of aging which is a risk factor of AD. These results potentially point TRPM2 channel to be involved in AD through glial cells. This review summarizes recent advances in studying the contribution of TRPM2 in health and in AD pathology, with a focus on contributions via glia cells.