There was an error in Development (2015) 142, dev115568 ().
![Loss of Fgfr2b, but not Fgfr1b, results in decreased inhibitory presynaptic differentiation in hippocampal CA3 in vivo. (A-C) Decreased inhibitory presynaptic differentiation (VGAT immunostaining) in CA3 of Fgfr2b+/− mice compared with WT at P8. (A) Representative images. (B) Quantification of VGAT intensity, normalized to WT littermates. (C) VGAT puncta size and density in SL [n=(sections, animals) 77, 5 Fgfr2b+/−; 52, 3 WT]. (D-F) No change in inhibitory presynaptic differentiation (VGAT immunostaining) in hippocampal CA3 of Fgfr1b−/− mice compared with WT at P8. (D) Representative images. (E) Quantification of VGAT intensity, normalized to WT littermates. (F) VGAT size and density in SL [n=(sections, animals) 71, 6 Fgfr1b−/−; 71, 6 WT]. (G,H) Loss of one copy of Fgfr1b does not exacerbate inhibitory presynaptic defects in Fgfr2b+/− mice. (G) Representative images. (H) VGAT intensity, relative to WT littermates [n=(sections, animals) 15, 5 Fgfr2b+/−Fgfr1b+/−; 14, 5 Fgfr2b+/−; 12, 4 WT]. Scale bars: 15 µm.](https://cob.silverchair-cdn.com/cob/content_public/journal/dev/151/16/10.1242_dev.203123/1/dev20312301.png?Expires=1750184920&Signature=me3FYWSkcJu0jhEzqLImjHT3VqAxNcp5e9cUFqLGpc-3uVNQgvZSUD0nl0pu0-Gfm40YcLwpLVRj7TFwLorX3giJ0X78Z8JuNLMxwmWtDVhIz0k6r~Xy0Lbyxsc~2xbQgsc~dVlPn-Q219-h2qc3DR7vT~TZfOk7GVxnXnuaW-cxy1K-2LS1yOLuxn3fkFJDlNvEHGpRORNq2moiYz4oWiwzD3omthxEgWsLD7wZHE2wlLTVhmuSiHkdRe-Ou-xX3JHfPG-xS2p4Gevx3pLcTKNBV0kalDH~YCqssWwdz~aQ6-EKuf~QKIWTE8G~lrLZYAdJbcdJ~YUP7VWxB2-yzg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Loss of Fgfr2b, but not Fgfr1b, results in decreased inhibitory presynaptic differentiation in hippocampal CA3 in vivo. (A-C) Decreased inhibitory presynaptic differentiation (VGAT immunostaining) in CA3 of Fgfr2b+/− mice compared with WT at P8. (A) Representative images. (B) Quantification of VGAT intensity, normalized to WT littermates. (C) VGAT puncta size and density in SL [n=(sections, animals) 77, 5 Fgfr2b+/−; 52, 3 WT]. (D-F) No change in inhibitory presynaptic differentiation (VGAT immunostaining) in hippocampal CA3 of Fgfr1b−/− mice compared with WT at P8. (D) Representative images. (E) Quantification of VGAT intensity, normalized to WT littermates. (F) VGAT size and density in SL [n=(sections, animals) 71, 6 Fgfr1b−/−; 71, 6 WT]. (G,H) Loss of one copy of Fgfr1b does not exacerbate inhibitory presynaptic defects in Fgfr2b+/− mice. (G) Representative images. (H) VGAT intensity, relative to WT littermates [n=(sections, animals) 15, 5 Fgfr2b+/−Fgfr1b+/−; 14, 5 Fgfr2b+/−; 12, 4 WT]. Scale bars: 15 µm.
Loss of Fgfr2b, but not Fgfr1b, results in decreased inhibitory presynaptic differentiation in hippocampal CA3 in vivo. (A-C) Decreased inhibitory presynaptic differentiation (VGAT immunostaining) in CA3 of Fgfr2b+/− mice compared with WT at P8. (A) Representative images. (B) Quantification of VGAT intensity, normalized to WT littermates. (C) VGAT puncta size and density in SL [n=(sections, animals) 77, 5 Fgfr2b+/−; 52, 3 WT]. (D-F) No change in inhibitory presynaptic differentiation (VGAT immunostaining) in hippocampal CA3 of Fgfr1b−/− mice compared with WT at P8. (D) Representative images. (E) Quantification of VGAT intensity, normalized to WT littermates. (F) VGAT size and density in SL [n=(sections, animals) 71, 6 Fgfr1b−/−; 71, 6 WT]. (G,H) Loss of one copy of Fgfr1b does not exacerbate inhibitory presynaptic defects in Fgfr2b+/− mice. (G) Representative images. (H) VGAT intensity, relative to WT littermates [n=(sections, animals) 15, 5 Fgfr2b+/−Fgfr1b+/−; 14, 5 Fgfr2b+/−; 12, 4 WT]. Scale bars: 15 µm.
In Fig. 2D, the wild-type (WT) representative image was erroneously a duplication of the Fgfr1b–/– image. A replacement panel from the original data has been substituted. The corrected Fig. 2 is shown below.
The authors apologize for this error, which does not impact the results and conclusions of the paper.
