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. 2017 Jun 15;7:3575. doi: 10.1038/s41598-017-03909-0

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Glycine treatment reduces cell loss in the ischemic brain where NMDAR channel activity and glycine receptors are inhibited. (A) Sample images of FJC strained-brain sections collected at 3 d after ischemia onset. Glycine (100 µg/100 g, icv) was administered at 3 h following I/R. At 30 min prior to glycine injection, MK-801 (8.0 µg/100 g, icv) and strychnine (1.2 µg/100 g, icv) were injected. (B) The bottom panel is a higher magnification of three regions in the upper panel marked with a frame. Bar = 100 μm. (C) Quantitative analysis of FJC-positive degenerating neurons in the ischemic brain area at 3 d after ischemia onset (n = 6, ANOVA test, *P < 0.05 vs. I/R + Stry + MK). Stry: Strychnine; Gly: glycine; MK: MK-801.