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. Author manuscript; available in PMC: 2022 Feb 19.
Published in final edited form as: Nat Neurosci. 2021 Aug 19;24(10):1377–1391. doi: 10.1038/s41593-021-00913-6

Figure 6. PI3K inhibitors, not an mGluR5 antagonist, rescue neurodevelopmental defects in FXS organoids.

Figure 6.

Both control and FXS-derived forebrain organoids were treated by pan-PI3K inhibitor LY294002 (10 μM), selective PI3Kβ inhibitor GSK2636771 (1 μM), mGluR5 antagonist MPEP (10 μM), or DMSO (vehicle) from day 42 to day 56 for two weeks. (a-b) Inhibition of PI3K increases NPC proliferation in FXS organoids. Representative images (a) and quantification (b) of the proportion of Ki67+ neuronal progenitor cells under different treatment conditions in both control and FXS-derived forebrain organoids at day 56. Data are presented as mean ± s.d. (n = 30 sections from at least from 10 organoids each condition; ****P < 0.0001, two-way ANOVA). Scale bars: 50 μm. (c-d) Inhibition of PI3K recues deficit of synaptic formation in FXS organoids. Shown are sample images (c) and quantification (d) of SYN1+PSD95+ puncta density under different treatment conditions in both control and FXS-derived forebrain organoids. Data are presented as mean ± s.d. (n = 30 sections from at least from 10 organoids each condition; ***P = 0.0002, ****P < 0.0001, two-way ANOVA). Scale bars: 50 μm.

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