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. 2019 Apr 24;39(17):3204–3216. doi: 10.1523/JNEUROSCI.2996-18.2019

Figure 7.

Figure 7.

Genetic coupling between NgR1 and PlexinA2 limits corticospinal axon sprouting after injury. A, Schematic image of unilateral pyramidotomy surgery. B, PKC γ density in dorsal columns at cervical cord coronal sections from PyX mice was imaged. The intact side is bright and the lesioned side shows little or no staining. C, Each marker shows percentage of density of injured side relative to intact side in each animal. Data are also presented as mean with SEM. No significant differences between groups with one-way ANOVA followed by Tukey's test. D, Representative image of BDA traced fibers in cervical spinal cord. Scale bars, 500 μm. Right, High-magnification view of white boxes shown in images. E, The graph shows the length of CST axons in gray matter on the denervated side of the cervical spinal cord. Values are normalized by the intact side axon length in the same sections from pyramidotomized WT (n = 9), NgR1+/− (n = 8), PlexinA2+/− (n = 7), and NgR1+/−PlexinA2+/− (n = 7) mice. Error bars represent SEM. *p < 0.05, one-way ANOVA followed by Tukey's multiple-comparisons test. Results for four sections from each mouse were averaged to create one value for each of n mice. F, The graph shows the number of midline crossing of uninjured CST axon from pyramidotomized WT (n = 9), NgR1+/− (n = 8), PlexinA2+/− (n = 7), and NgR1+/−PlexinA2+/− (n = 7) mice. Error bars represent SEM. n.s., not significant, *p < 0.05, one-way ANOVA followed by Tukey's multiple-comparisons test.