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. 2019 Nov 29;2:446. doi: 10.1038/s42003-019-0694-x

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© The Author(s) 2019

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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Fig. 3 — a, b The model of active formaldehyde-activated NMDA-R by binding to C232 residue of NR2B. Ifenprodil (Ifen, a specific antagonist of NR2B). FA formaldehyde. c The chemical equation between formaldehyde and l-cysteine. d, e Recording of NMDA currents in CHO cells cotransfected with GFP-NR1a and NR2B without the amino terminal domain (NR2B-ATD) or a single point mutation (C232A). LBD ligand binding domain. n = 10−12. f, g The model of excessive formaldehyde-suppressed NMDA-R by cross-linking C79 of NR1 to K79 of NR2B. h, i Recording of NMDA currents in CHO cells cotransfected with C79S mutant NR1a and/or K79S mutant NR2B, respectively (n = 10−12). The data are expressed as the mean ± standard error (s.e.m.). ***p < 0.001; ****p < 0.0001.