Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Dec 10;13:7656. doi: 10.1038/s41467-022-35417-9

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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/.

PMC Copyright notice

Fig. 8 — Α Schematic and representative traces illustrating that retrograde PHP signaling is occluded at NMJs containing chimeric GluRB receptors, while PHP is robustly expressed at NMJs containing wild-type GluRB receptors. Note that while mEPSP amplitudes are similarly reduced at NMJs containing only GluRB receptors, the presynaptic release does not increase when pCaMKII is recruited to NMJs by chimeric GluRB receptors. B Quantification of mEPSP and quantal content values in the indicated genotypes normalized to wild-type values (wild type: n = 12; GluRIIA^−/−, n = 10, p < 0.0001 for mEPSP, p < 0.0001 for QC; G14 > GluRIIB: n = 11, p < 0.0001 for mEPSP, p < 0.0001 for QC; G14 > GluRIIB^IIAtail: n = 12, p < 0.0001 for mEPSP, p = 0.4908 for QC). C–E Quantification of average mEPSP amplitude (C), EPSP amplitude (D), and quantal content values (E) in the indicated genotypes (wild type: n = 12; GluRIIA^−/−, n = 10, p < 0.0001 for mEPSP, p = 0.331 for EPSP, p < 0.0001 for QC; G14 > GluRIIB: n = 11, p < 0.0001 for mEPSP, p = 0.596 for EPSP, p < 0.0001 for QC; G14 > GluRIIB^IIAtail: n = 12, p < 0.0001 for mEPSP, p < 0.0001 for EPSP, p = 0.490 for QC). Repeated measures one-way ANOVA with Dunnett’s multiple comparisons test with a significance value of 0.05. p Value adjusted for multiple comparisons. F Schematic summarizing that active pCaMKII is lost from postsynaptic compartments due to the physical absence of the GluRIIΑ C-tail. This, in turn, releases the inhibition of retrograde PHP signaling. Error bars indicate ±SEM. ****p < 0.0001; ns, not significant. n values indicate biologically independent NMJs. Absolute values for normalized data are summarized in Table S1. Source data are provided as a Source Data file.