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. 2017 Jan 15;28(2):285–295. doi: 10.1091/mbc.E16-07-0526

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© 2017 Szíber et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 6: — Anti-GluA1 antibody feeding in hippocampal neuronal cultures. Relative anti-GluA1 signal intensity was determined within Shank2-positive postsynaptic densities (PSDs) at the plasma membrane. (A) Representative pictures of Rin1⁻^/⁻ dendrites transfected with EGFP or EGFP-tagged RIN1^WT after 10 min of antibody feeding with anti-GluA1. PSD was delineated based on clear Shank2 positivity. Arrows point at shaft synapses; arrowheads indicate spines. Scale bar, 1 μm. (B–D) Quantification of GluA1 signal intensities within Shank2-positive PSD areas in EGFP-transfected neurons of CD1 cultures (C) or in Rin1⁻^/⁻ neurons transfected with the indicated EGFP-tagged constructs (B, D). cLTD was evoked by 3 min of 50 μM NMDA treatment, and neurons were analyzed 2 h later (C, D). Imatinib was applied at 5 μM for 1 h (B). Data are presented as mean ± SEM. *^,$p < 0.05; **p < 0.01; ***^,$$$p < 0.001. Asterisk indicates difference compared with the EGFP values.