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. 2015 Nov 4;35(44):14794–14808. doi: 10.1523/JNEUROSCI.1295-15.2015

Figure 6.

Figure 6.

5-HT mediates axon guidance through ephrinB2a (efnB2a). A, The efnB2ahu3393 allele is a nonsense mutation in the receptor-binding domain (exon 2) of ephrinB2a (T>A; C86X). SP, Signal peptide; RBD, receptor-binding domain; TM, transmembrane domain. B–K, M, M′, Confocal images, rostral top. Scale bar, 50 μm. B, C, efnB2 immunohistochemistry. efnB2 protein is absent in the efnB2ahu3393/hu3393 (efnB2a−/−) embryo compared with WT. D–G, Acetylated tubulin immunohistochemistry does not show gross axon defects in efnB2a−/− embryos. D, E, Axons in dorsal brain. F, G, Axons in ventral brain. H–K, GFP immunohistochemistry in Tg(foxP2-enhancerA.2:egfp-caax) embryos shows that lack of efnB2 (in efnB2a−/− embryos; J, K) prevents ketanserin-induced midline crossing defects (arrow) compared with efnB2a heterozygotes (H, I). L, Quantification confirms that efnB2a−/− restores axon guidance in presence of ketanserin. n = 10 per group. *p < 0.05, two-way ANOVA followed by Bonferroni post test. Error bars indicate SEM. M, efnB2a−/− mutant has normal raphe 5-HT expression compared with WT (M′). N, Scatterplot of C/L1 raw data results for L.