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. 2016 Mar 24;7:11096. doi: 10.1038/ncomms11096

Figure 4. Temporal-specific rescue of eB3 restores defensive responses in Efnb3−/− mutant.

Figure 4

(a) Transgenic mice expressing tamoxifen-inducible Cre recombinase under the control of the CAGG promoter (CAGG-CreERT2M) were crossed with Efnb3−/− homozygotes. EB3 expression in the initial Efnb3−/− mutant is restored on tamoxifen administration to induce Cre-mediated excision of the loxP-flanked PGK neo cassette. (b) Schedule of tamoxifen treatment and brain perfusion during postnatal development. All the mice including wild-type controls were treated with tamoxifen injection at the indicated time. (c) CAGG-Cre+; Efnb3−/− mice showed a shorter time in EPM open arms than CAGG-Cre; Efnb3−/− at P16 following tamoxifen treatment at P12 but not when tamoxifen was applied at P38. The experiments were triplicated independently. n values of mice used are indicated above group bars. *P<0.05, one-way ANOVA. (d) Representative images showing Thy1-GFP M-labelled axon bundles projecting into amygdala of CAGG-cre; Efnb3−/− and CAGG-cre+; Efnb3−/− mice. Scale bars, 100 μm. (e) Quantification of the total peak number of axonal GFP signal crossing the dotted line and fasciculated axonal bundles (indicated with red square brackets). n values of brain slices from 5 to 6 mice per group are indicated above each group bar, **P<0.01; ***P<0.001, one-way ANOVA.