Skip to main content
Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: GSK3β-mediated tau hyperphosphorylation triggers diabetic retinal neurodegeneration by disrupting synaptic and mitochondrial functions

Fig. 3

Intravitreal delivery of si-Tau restores HFD-induced RGCs dysfunction and synapse loss. si-Tau was injected in the vitreous of the right (R) eye of mice at 20 weeks after RD (RD-R-si-Tau) or HFD (HFD-R-si-Tau), while a scramble si-sc was injected in the contralateral (left; L) eye as a control (RD-L-si-sc; HFD-L-si-sc). (a) Representative waveforms of visual evoked potential (VEP). The differences in peak amplitude (N1-P1) were quantified. (b) Representative images of double immunostaining for phospho-tau (pS396- or pT231-Tau; green) with total-tau (Tau-5; red), and for synaptophysin (green) with Tau 5 (red). Scale bar, 100 μm. (c) Representative curvilineal profile of protein immunostaining intensity from GCL to OPL across retinal depth of the images shown in B. Data are means ± SEM. n = 5 eyes per group. For each eye, data from three independent curvilineal diagrams were averaged, and the mean of five eyes was used as the representative value for each group. **P < 0.01 vs contralateral eye injected with si-sc. NS, no significant difference

Back to article page