FIGURE 7.

Morphologic and immunohistochemical characterization of the retina from light-exposed (EM108, OS; EM112, OS) and shielded (EM112, OD) T4R RHO mutant dogs; dog EM108 was treated with systemic DEX, and dog EM112 was not treated. All sections from an individual eye were from a series of serial sections taken from the same region. (A₁) Marked thinning of the ONL, and loss of photoreceptor inner and outer segments in the DEX-treated, light-exposed mutant retina. Note the preservation of the RPE (arrows). (B₁) Similar loss of photoreceptors in the untreated, light-exposed retina. Note, however, the absence of the RPE. (C₁) Normal retinal structure and lamination in the shielded eye. (A₂) Weak RPE65 labeling (arrows; green) and absence of GFAP labeling (red) in the DEX-treated light-exposed mutant retina. (B₂) Strong GFAP labeling in the untreated, light-exposed retina; the absence of RPE65 labeling resulted from RPE loss. (C₂) The shielded mutant retina was normal, and RPE labeling was intense and distinct. (A₃) The majority of the remaining cell somata in the ONL of the DEX-treated, light-exposed mutant retina were human cone arrestin (hCAR) positive (arrowheads; red); punctate labeling of some cells with the rod opsin antibody is also present (arrows; green). (B₃) Similar findings in the untreated, light-exposed retina. (C₃) Normal pattern of rod opsin (green) and hCAR (red) labeling in the shielded mutant retina. TL, tapetum lucidum; OS, outer segments; IS, inner segments; INL, inner nuclear layer; GCL, ganglion cell layer. Scale bar, 20 μm.