Skip to main content
. 2015 May 28;112(23):E3010–E3019. doi: 10.1073/pnas.1505870112

Fig. 6.

Fig. 6.

Loss of PRDM8 alters AC-subtype identity. Confocal micrographs of retinal cryosections from adult Prdm8EGFP/EGFP mice and WT littermates stained for AC markers. (A and B) Fewer GAD65+ ACs in the INL and decreased GAD65 IPL staining were present in the Prdm8EGFP/EGFP retina, specifically of the middle and innermost GAD65+ bands of the IPL. (AA″) PRKCA+ ACs colocalized with a subset of weakly positive GAD65+ cells in WT retina (arrows). (BB″) In the Prdm8EGFP/EGFP retina, PRKCA+ AC numbers were significantly increased; some PRKCA+ cells were GAD65+ (arrows), whereas others expressed very low intensity or no GAD65 (arrowheads). (C) CHAT+ cholinergic AC bodies and their processes did not coexpress PRKCA in WT retina. (D) In Prdm8EGFP/EGFP retina, both CHAT+ and PRKCA+ ACs were increased in number, but the two populations remained distinct. (EF′) VGLUT1 labels axon terminals of BP cells, and calretinin labels a subset of ACs, which together help to define the five sublaminae of the IPL. (E and F) Lamination was maintained in Prdm8EGFP/EGFP retina, but the density of VGLUT1 staining in each sublamina was reduced, and the layers appeared to be thinner. (E′ and F′) Enlargement of IPL areas described in E and F.