PERG analysis, a sensitive measure of visual function in the mice was used to monitor optic neuritis in unsensitized control mice intravitreally injected with scAAV-
mCherry, EAE-sensitized mice injected with scAAV-
mCherry, and EAE-sensitized mice injected with scAAV-
NDUFA6Flag. At 1 month post sensitization we found no significant differences in mean PERG amplitudes (
Fig. 2A) and latencies (
Fig. 2B) among the groups. By 3 months the EAE-
mCherry mice showed a significant reduction in the PERG amplitude (43%,
P = 0.0099) and a delay in latency (19%,
P = 0.0305) compared with unsensitized control-
mCherry mice. In contrast,
NDUFA6Flag-protected mice showed a complete suppression of the amplitude loss (
P < 0.0001) and the delay in latency (
P = 0.0011). At 6 months post sensitization, EAE-
mCherry mice showed a significant reduction in amplitude (44%,
P = 0.0035) and delay in latency (21%,
P = 0.0378) compared with unsensitized control
mCherry mice. However, PERG amplitudes and latencies of mice that were injected with
NDUFA6Flag were comparable to unsensitized control
mCherry mice (
P > 0.05) who were not sensitized for EAE. Compared with the EAE-
mCherry group, NDUFA6 treatment significantly suppressed the amplitude loss (76.5%,
P = 0.0039) and the latency delay (76%,
P = 0.043). Mean PERG waveforms showed the loss of amplitude and delay in latency associated with EAE were rescued with
NDUFA6Flag injection (
Fig. 2C). The mean PERG amplitudes ± SE and latencies ± SE at 1, 3, and 6 months post injection and the corresponding
P values are listed in
Supplementary Tables S1 and S2, respectively. Overall, there was a progressive loss of visual function in EAE-sensitized mice and NDUFA6FLAG overexpression preserved visual function. None of the DBA/1J mice sensitized for EAE developed paralysis.