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. 2021 Sep 16;14:143. doi: 10.1186/s13041-021-00848-w

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 4 — Surface GluA1 is increased in VKI and altered by acute LRRK2 kinase inhibition. A GFP-filled (cyan) cultured cortical cells immunostained for MAP2 (blue; to ensure no permeabilization) and surface GluA1 (magenta) (i, left panel); in silico neurite outlines with only GluA1 staining displayed (i, right panel). There was a significant genotype effect on GluA1 cluster density, due to opposing effects on heterozygous and homozygous cells (ii, Kruskal–Wallis p < 0.009; Uncorrected Dunn’s Het-Ho *p < 0.05). There was a significant genotype effect on surface GluA1 cluster intensity (synaptic GluA1) due to significant increases in heterozygous cells (iii, Kruskal–Wallis p < 0.007; Uncorrected Dunn’s Het **p < 0.02). B GFP-filled cultured cortical neurons from WT mice treated with saline or Captisol and immunostained for MAP2 (blue), GFP (cyan), and extracellular GluA1 (magenta) without permeabilization. There were no effects of Captisol treatment on surface GluA1 cluster density (ii, Unpaired t-test p = 0.87) or intensity (iii, Mann–Whitney p = 0.73). C Non-permeabilized cultured cortical cells immunostained for MAP2 (blue), and surface GluA1 (magenta) following acute MLi-2 or vehicle treatment (i). Changes to GluA1 surface density after treatment showed a significant genotype effect due to increases in WT cells not observed in heterozygous and homozygous mutant cells (ii, Welch’s ANOVA p < 0.0002; Unpaired t with Welch’s correction WT-Het **p < 0.003; WT-Ho ****p < 0.0001). There was a significant genotype effect on change in surface GluA1 intensity following treatment, due to opposing increases in heterozygous cells and decreases in WT and homozygous cells (iii, Kruskal–Wallis p < 0.02; WT-Het *p < 0.02; Het-Ho *p < 0.02)