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. 2022 Jul 15;13:4114. doi: 10.1038/s41467-022-31817-z

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© The Author(s) 2022

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–d Chemical structures of uncharged forms of additional NMDAR channel blockers examined (left); examples of current traces during MCI protocols performed at pH 7.2 using GluN1/2A receptor-expressing tsA201 cells; overlays of I_Control and I_MCI (I_MCI in red); I_MCI/I_Control point-by-point ratios (right). Concentrations and blockers tested: 10 μM phencyclidine (PCP; a); 1 μM MK-801 (b), 50 μM dextrorphan (Dex; c), 20 μM RL-208 (d). e Examples of current trace during MCI protocol performed with 1 μM MK-801 at pH 7.2 using neurons in primary culture, overlay of I_Control and I_MCI (I_MCI in red), and I_MCI/I_Control point-by-point ratio (right). 50 μM APV was applied from 1 s before until 0.2 s after MK-801 application to ensure that channel openings during MK-801 application (which could allow traditional channel block) did not occur. All solutions used for neuronal recordings contained 1 μM tetrodotoxin and 1 μM Ro 25-6981; NMDARs were activated by application of 100 μM NMDA. In b and e a 20 s to 30 s V_m step to 30 mV was performed after MK-801 application to speed unbinding from the deep site, allowing full recovery from MK-801 inhibition (needed because MK-801 has a much slower unbinding rate at −65 mV than the other blockers). f Min I_MCI/I_Control based on the protocols shown in a–e for 10 μM PCP (0.409 ± 0.063, n = 5), 1 μM MK-801 (0.459 ± 0.035, n = 4), 50 μM dextrorphan (0.549 ± 0.043, n = 4), and 20 μM RL-208 (0.275 ± 0.017, n = 3) applied to tsA201 cells, and 1 μM MK-801 (0.612 ± 0.019, n = 3) applied to cultured neurons. Min I_MCI/I_Control values were compared to 1 with two-sided t-test; all are significantly different from 1 (PCP, t = −9.36, df = 4, p = 0.00073; MK-801 with GluN1/2A receptors, t = −15.5, df = 3, p = 0.00059; Dex, t = −10.5, df = 3, p = 0.0019; RL-208, t = −43.4, df = 2, p = 0.00053; MK-801 with neurons, t = −28.3, df = 2, p = 0.0013). Mean ± SEM is plotted.