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. 2014 Jul 23;2(1):8. doi: 10.1186/2050-490X-2-8

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© Shu et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Blockade of NMDA receptor or NMDA-DAPK1 downstream signaling induces different fates of neuronal cells in stroke. (A) Blockade of NMDA receptor in stroke causes 1) inhibition of necrosis, apoptosis and autophagy of neuronal cells; 2) suppression of endogenous surviving and regeneration signaling; 3) interruption of physiological functions of synaptic transmission. (B) Blockade of NMDA(NR2B)-DAPK1 downstream signaling in stroke specifically mediates 1) prevention of cell death (such as necrosis, apoptosis and autophagy); 2) probable inhibition of cell survival; and 3) no adverse effects on physiological functions of synaptic transmission.