IJPPP Copyright © 2009-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711
Int J Physiol Pathophysiol Pharmacol 2012;4(4):211-218

Review Article
Differential roles of GluN2A- and GluN2B-containing
NMDA receptors in neuronal survival and death

Brendan Lujan, Xiaoxuan Liu, Qi Wan

Department of Physiology and Cell Biology, University of Nevada School of Medicine, 1664 North Virginia Street,
MS0352, Reno, NV 89557, USA

Received December 14, 2012; Accepted December 25, 2012; Epub December 26, 2012; Published December
31, 2012

Abstract: Glutamate-induced neurotoxicity is the primary molecular mechanism that induces neuronal death in a variety of pathologies
in central nervous system (CNS). Toxicity signals are relayed from extracellular space to the cytoplasm by N-methyl-D-aspartate
receptors (NMDARs) and regulate a variety of survival and death signaling. Differential subunit combinations of NMDARs confer
neuroprotection or trigger neuronal death pathways depending on the subunit arrangements of NMDARs and its localization on the cell
membrane. It is well-known that GluN2Bcontaning NMDARs (GluN2BRs) preferentially link to signaling cascades involved in CNS
injury promoting neuronal death and neurodegeneration. Conversely, less well-known mechanisms of neuronal survival signaling are
associated with GluN2A-comtaining NMDARs (GluN2AR)-dependent signal pathways. This review will discuss the most recent
signaling cascades associated with GluN2ARs and GluN2BRs. (IJPPP1212003).

Keywords: NMDA receptor, GluN2A, GluN2B, neuronal survival, neuronal death

Address all correspondence to:
Dr. Qi Wan
Department of Physiology & Cell Biology
University of Nevada School of Medicine
Center for Molecular Medicine
Room L-207D, 1664 North Virginia Street, MS0575,
Reno, NV 89557, USA.
Phone: 775-7844352 (O); 775-7844351 (Lab)
E-mail: qwan@unr.edu