Figure 9.
The C terminus is necessary for the function of Cx43 during neuronal migration. At E14, Tα1–GFP plasmid was injected alone or coinjected with CMV–Cx43 plasmid into the lateral ventricle of Cx43−/−, Cx43K258stop/+, or Cx43K258stop/− mice, followed by electroporation (a–d). Four days later, the electroporated brains were removed, 10 μm sections of cerebral cortices were collected, and subsequently the GFP+ cells were visualized under an epifluorescent microscope. Although in Cx43K258stop/− mice neurons failed to migrate to the CP (a), Cx43K258stop/+ mice showed normal neuronal migration (b). The bar graph on the right indicates a significant difference in neuronal migration between Cx43K258stop/− and Cx43K258stop/+ mice. In Cx43−/− mice, neurons electroporated with Tα1–GFP failed to migrate to their final location in the CP (c), whereas CMV–Cx43 rescued neuronal migration in these mice (d). The bar graph on the right shows that the percentage intensity of GFP in the CP of Cx43−/− mice, rescued with CMV–Cx43, is significantly higher than of those injected with only Tα1–GFP. Disrupted neuronal migration by Cx43siRNA is shown in e and f. In Cx43+/+ mice, 4 d after electroporation, cells transfected with Cx43–siRNA were positioned in the VZ/IZ, and no cells reached the CP (e), whereas cells transfected with control–siRNA were able to migrate to the CP (f). The bar graph on the right demonstrates that Cx43–siRNA causes a significant loss in the CP when compared with the control–siRNA. *p < 0.05, Student's t test. n = 3. Scale bars, 200 μm.