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. Author manuscript; available in PMC: 2016 May 20.
Published in final edited form as: Neuron. 2015 May 7;86(4):985–999. doi: 10.1016/j.neuron.2015.04.005

Figure 3. Loss of CNTN4 results in a decrease of innervation by Hoxd10-GFP RGC axons to the NOT.

Figure 3

(A–F) Hoxd10-GFP RGC axons in the NOT at P8 (A–C) and at P20 (D–F), in wildtype (A, D), CNTN4+/− (B, E), and CNTN4−/− mice (C, F). Scale = 250μm; D = dorsal; L = lateral.

(G) Fraction of the termination zone (in NOT) occupied by Hoxd10-GFP RGC axons in wildtype (black), CNTN4+/− (dark grey) and CNTN4−/− (light grey) mice (±SEM). *= p<0.05 (n=4–6 mice per genotype, per age).

(H) Total number of Hoxd10-RGCs in the retinas of wildtype and CNTN4−/− mice at P8 (±SEM). n= 5–6 mice per genotype.

(I–J) RGC axons in NOT of wildtype (I) and CNTN4−/− mice (J) labeled by intraocular CTβ-594. Scale = 200μm.

(K) Total volume of the NOT (mm3 ±SEM) in wildtype (black) and CNTN4−/− mice (grey) (n = 3 mice per genotype).

(L–Q) DRD4-GFP RGC axons in the NOT at P8 (L–N) and at P20 (O–P), in wildtype (L, O), CNTN4+/− (M, P) and CNTN4−/− mice (N,Q). Scale = 250μm.

(R) Fraction of the termination zone (in NOT) with DRD4-GFP RGC axons in wildtype (black), CNTN4+/− (dark grey) and CNTN4−/− (light grey) mutants (±SEM).

*= p<0.05 **=p<0.01, (n=5–6 mice per genotype, per age).