Fig. 6.

Prolonged depolarization of ependymal glial cell membrane using ivermectin or glycine inhibits axon regeneration across the injury site. Spinal cords were injected with either vehicle control PBS (A), or the GlyCl-R agonists IVR (B) or the native ligand for GlyCl-R glycine (C) immediately before spinal cord ablation. Activation of GlyCl-R causes Cl⁻ efflux leading to chronic depolarization. In control animals 7 days post injury the axons have regrown through the injury site, as visualized using whole mount anti-β III tubulin staining (A, A′). In animals where the ependymal glial cells were kept in a prolonged state of membrane depolarization by injection of ivermectin, axon regeneration was inhibited (B, B′). Injection of the native ligand for glycine gated chloride channels, glycine, phenocopied the drug phenotype (C, C′). * denotes injury site. Control N=47, Ivermectin N=32, Glycine N=17.