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. 2017 Nov 22;11:373. doi: 10.3389/fncel.2017.00373

Figure 5.

Figure 5

Propofol treatment disrupted the contacts between Purkinje cells and Bergmann glial cells at P8. (A–L) Immunolabeling for calbindin (green), GFAP (red), 4′,6-diamidino-2-phenylindole (DAPI) (blue), their merged images and respective high-resolution images of the merges in the cerebellar lobe IX. (A–C) Calbindin-stained Purkinje cells from the (A) Vehicle, (B) Propofol (30 mg/kg) and (C) Propofol (60 mg/kg) groups. (D–F) GFAP-stained Bergmann glial cell fibers from the (D) Vehicle, (E) Propofol (30 mg/kg) and (F) Propofol (60 mg/kg) groups. (G–I) The merged images showing the calbindin staining, GFAP staining and DAPI in the PCL. (J–L) Magnified images of panels (G–I) show the relationship between the calbindin-positive cells and GFAP-positive cells. The arrows indicate that the tips of calbindin-immunopositive dendrites are intimately attached to the rod-like shaft of Bergmann fiber contacting domains (M) Quantification of the numbers of contact points between the GFAP-positive fibers and calbindin-positive cells around the border between the ML and EGL in the identical lobe of the cerebellum. Data are presented as the mean ± SD (n = 5). Scale bar: (A–I): 50 μm and (J–L): 25 μm. **P < 0.01.