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. 2019 Nov 19;9:17078. doi: 10.1038/s41598-019-53225-y

Figure 1.

Figure 1

PKCγ is phosphorylated in intact CST after unilateral TBI. (a) Simplified schematic illustration of unilateral TBI, CST degeneration and plasticity. Unilateral TBI causes cortical injury which affects CST degeneration (red dotted lines). CST from the contralesional, intact cortex sprouts axons that cross the midline into the denervated spinal cord after TBI (green lines). This sprouting can be anterogradely labelled by CST tracer. (b) Unilateral TBI of left cortex destroyed the right dorsal CST (dCST) in the cervical spinal cord. Cervical spinal cord sections derived from 2 weeks post-injured mice were immunostained with SMI-31 or MAG antibody. The lower panel showed the relative immune-intensity of right dCST to the contralateral dCST. (c) Immunofluorescence (IF) staining showed an increase of p-PKCγ expression in left dCST and a decrease in the right dCST in the cervical spinal cord after TBI. The immune-intensity of p-PKCγ in the left or right dCST was compared to homolateral dCST in Sham spinal cords. Data are expressed as mean ± SD (n = 3 animals in each group) and compared by Student’s t-test (**p < 0.01 vs Sham). Scale bars, 50 μm.