Figure 4.

Injury increases gap junction coupling between ependymal cells of the adult spinal cord. A, Experimental design to search for plasticity of ependymal cell functional properties in early stages after injury. Bottom right, Collage of a living spinal cord slice at 5 DPI. B, RMP (B₁, RMP), IR (B₂, IR), and ratio of Type 1 and Type 2 cells (B₃) in ependymal cells from sham-injured (sham) and injured (5 DPI) adult spinal cord. The IR between the two groups was significantly different (p < 0.05), whereas both the RMP and the proportion of Type 1 and Type 2 cells were not. C, Single ependymal cell recorded at 5 DPI (stack of 7 confocal optical sections). Recombination of tdTomato confirms the ependymal identity of the recorded cell. D, Cluster of dye-coupled cells at 5 DPI covering the dorsolateral (D₁), ventrolateral (D₂), and ventral (D₃) aspects of the CC (stacks of 47, 21, and 25 optical sections, respectively). D₃, The cluster has a bundle of processes projecting to the ventral sulcus (arrowhead). D₃, Inset, The expression of tdTomato in ependymal cells shows the cluster was within the ependymal cell layer. E, Large cluster of dye-coupled cells spanning the lateral domain of the CC at 5 DPI (E₁, stack of 22 optical sections). Most of dye-coupled cells matched the expression of tdTomato. The cluster corresponded to a Type 1 cell phenotype (E₂). Cbx (100 μm) increased the apparent IR of the recorded cell, suggesting the gap junction coupling with neighboring cells (E₃). F, The proportion of clusters of dye-coupled ependymal cells over single cells was significantly higher (p < 0.01) at 5 DPI than in sham-injured animals. G, The volume of clusters of gap junction-coupled cells was similar in the CC of sham-injured and injured spinal cord (p = 0.48). *p < 0.05, **p < 0.01, ns = non significant.