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. 2015 Sep 15;26(18):3275–3288. doi: 10.1091/mbc.E15-02-0093

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© 2015 Koles 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 2: — Past1 mutants have reduced postsynaptic responses and defective homeostatic compensation. (A) Past1 mutants have reduced GluRIIA levels but normal GluRIIB and GluRIIC levels. Maximum intensity projections of 60× spinning-disk confocal stacks from a representative muscle 4. Scale bar, 2 μm. (B) Quantification of GluR levels from 3D volumes surrounding HRP staining. (C) Normal presynaptic (α-BRP) and postsynaptic (α-GluRIIC) apposition in past1 mutants. Maximum intensity projections of 100× spinning-disk confocal stacks from a representative muscle 4. Scale bar, 10 μm. (D) Representative traces from muscle recordings. The x-axis scale bar, 50 ms (EPSPs), 10,000 ms (mEPSPs); y-axis scale bar, 5 mV (EPSPs), 1 mV (mEPSPs). (E–H) Quantification of electrophysiological phenotypes. (E) mEPSP amplitude, (F) EPSP amplitude, (G) mEPSP frequency, and (H) quantal content, adjusted for nonlinear summation (NLS). Genotypes include white (wild type), n = 31; past1^60-4/110-1, n = 13; GluRIIA^SP16, n = 44; and GluRIIA^SP16; past1^60-4/110-1, n = 16.