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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-GluN1 binding antagonist and Akt inhibitor attenuate the effect of glycine in reducing the infarct volume after glycine receptors and the channel activity of NMDARs are inhibited. (A) Sample images of TTC strained-brain sections collected at 24 h after ischemia onset. Glycine (100 µg/100 g, icv) was administered at 3 h following I/R. Glycine-GluN1 binding antagonist L-689560 (L68; 0.1 mg/100 g, ip) or Akt inhibitor IV (100 µM, 2 µl, icv) is injected with MK-801 and strychnine at 30 min before glycine injection. (B) Summarized quantification data indicate that glycine-GluN1 binding antagonist and Akt inhibitor treatment attenuate the effect of glycine in reducing the infarct volume after glycine receptors and NMDARs are inhibited (n = 6, ANOVA test, *P < 0.05 vs. I/R + Stry + MK; ^# P < 0.05 vs. I/R + Stry + MK + Gly). Stry: Strychnine; Gly: glycine; MK: MK-801.