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. 2023 Mar 30;14:1771. doi: 10.1038/s41467-023-36872-8

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© The Author(s) 2023

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. 9 — a Mitral cells are infected with control or Dag1 gRNAs and tdTomato by projection-specific labeling through retro-AAVs injected in the piriform cortex. b Representative OB sections stained for gephyrin (green) and for tdTomato (red). c, d Dystroglycan deletion does not change the density or size of gephyrin-positive synapses (green) co-localized with tdTomato-expressing mitral cells (c, sample images; d, summary of puncta densities (top) and puncta size (bottom)). e Representative image of a mitral cell filled with neurobiotin (blue) and expressing tdTomato via AAVs (red). f–h Dystroglycan (Dag1) deletion decreases the mIPSC frequency in mitral cells (f, representative mIPSC traces; g, h cumulative probability of the mIPSC interevent intervals and amplitudes, insets: summary of the mIPSC frequency and amplitudes). i–k Dystroglycan (Dag1) deletion suppresses the IPSC amplitude at GC→MC synapses (i, representative IPSC traces; j, summary of input/output amplitudes; k, summary of the input/output curve slopes). l Mitral cell-specific dystroglycan (Dag1) deletion increases the coefficient of variation of evoked IPSCs. m, n Dystroglycan (Dag1) deletion induces a large increase in the paired-pulse ratio (m, representative traces; n, summary plot of the paired-pulse ratio). o–r Dystroglycan deletion in the mPFC decreases the mIPSC frequency monitored in Layer 5 pyramidal neurons (o, representative image of an mPFC section; p, representative mIPSC traces; q–r, cumulative probability of the mIPSC interevent intervals and amplitudes, insets: summary of the mIPSC frequency and amplitudes)). Numerical data are means ± SEM; n’s (animals (d) or cells/experiments (the rest)) are indicated in the summary graph bars (d) or above the sample traces (f, i, m, and p) and apply to all graphs in an experimental series with b–d belonging to the same series. Statistical analyzes were performed using two-tailed unpaired t-test in d, g, h, k, l, q, r, and by two-way ANOVA in j & n with Bonferroni multiple hypothesis testing, with *p < 0.05, **p < 0.01, and ***p < 0.001. Source data and statistical results for all experiments are provided within the Source Data file.