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Fig. 1 | Molecular Autism

Fig. 1

From: Deletion of Fmr1 in parvalbumin-expressing neurons results in dysregulated translation and selective behavioral deficits associated with fragile X syndrome

Fig. 1

De novo protein synthesis is elevated in PV and SOM-positive neurons in Fmr1−/y mouse hippocampus. A–B Representative images of FUNCAT in hippocampal slices from WT and Fmr1−/y mice, co-stained for either PV A or SOM (B, scale bar: 50 μm). C–D Quantification of PV labeling C or AHA fluorescence D in PV-positive WT and Fmr1−/y mouse hippocampal cells. Values represent mean ± SEM (n = 20–25 z-stacks, 9–11 sections, from 3 animals per genotype). E–F Quantification of SOM labeling E or AHA fluorescence F in SOM-positive WT and Fmr1−/y mouse hippocampal cells. Values represent mean ± SEM (n = 26–39 z-stacks, 11–13 sections from 3 animals per genotype). G Representative images of FUNCAT control in WT and Fmr1−./y mouse hippocampal slices where AHA was omitted; ***p < 0.0001 (Student’s t test)

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Molecular Autism

ISSN: 2040-2392