Fig. 1

Decreased RGCs activity in the absence of retinal microvasculopathy is associated with synaptic and axonal impairment occurring before RGCs apoptosis in HFD-induced diabetes. (a) Representative pattern electroretinography (PERG) waveforms of eyes in mice fed with regular chow (RD) or HFD for 20 and 24 weeks. Difference between peak-to-peak amplitude of P50 and N95 components (P50-N95) and the N95 peak latency were quantified. (b) Representative images of fundus fluorescein angiography. (c) Illustrative examples of retinal Evans Blue angiography. Right panels are high-power magnification of the areas indicated by the boxes. (d) Representative images of retinal immunostaining for apoptotic (TUNEL positive, green; indicated by arrow) cells. Nuclei were labeled with DAPI (blue). Scale bar, 100 μm. (e) Apoptotic RGCs were quantified and expressed as the percentage of TUNEL-positive cells to DAPI-positive cells in GCL. For each retinal section, the number of TUNEL positive cells in the GCL was counted. For each eye, results obtained from four independent sections were averaged. (f) Retinal immunofluoresence staining for synaptophysin (green, synaptophysin; blue, DAPI; scale bar, 100 μm). (g) Representative images for Golgi staining of RGCs axons at the proximal portions of optic nerves (black, indicated by arrow; scale bar, 10 μm) in longitudinal cryosections of optic nerves. Data are means ± SEM. n = 6 animals per group. ^**P < 0.01 vs age-match RD controls. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer