Figure 4
Figure 4. Inhibition of RGC-derived Sema3A during PR preserves neuroretinal function. (A) Representative recordings of full-field scotopic ERGs in response to progressively brighter flashes of white light ranging in intensity from −6.3 to 0.9 log cd/s/m2 in 0.3 log-unit increments (using a photostimulator with an interstimulus interval of 10 seconds, flash duration of 20 μs, and an average of 2-5 flashes). (B) Lv.shSema3A-treated mice show a significant gain in inner-retinal scotopic (mixed cone-rod) b-wave response (418.2 μV; n = 6) compared with control contra-lateral Lv.shGFP μV (234.3; n = 8) injected eyes. **P < .01 and ***P < .001 compared with corresponding controls. Similarly, knockdown of Sema3A enhances the response time to light stimulus, as illustrated by decreased peak times (56.4 ms) with respect to controls (67.1 ms). Inner retinal function as determined by a-wave amplitudes and peak times was not significantly affected.

Inhibition of RGC-derived Sema3A during PR preserves neuroretinal function. (A) Representative recordings of full-field scotopic ERGs in response to progressively brighter flashes of white light ranging in intensity from −6.3 to 0.9 log cd/s/m2 in 0.3 log-unit increments (using a photostimulator with an interstimulus interval of 10 seconds, flash duration of 20 μs, and an average of 2-5 flashes). (B) Lv.shSema3A-treated mice show a significant gain in inner-retinal scotopic (mixed cone-rod) b-wave response (418.2 μV; n = 6) compared with control contra-lateral Lv.shGFP μV (234.3; n = 8) injected eyes. **P < .01 and ***P < .001 compared with corresponding controls. Similarly, knockdown of Sema3A enhances the response time to light stimulus, as illustrated by decreased peak times (56.4 ms) with respect to controls (67.1 ms). Inner retinal function as determined by a-wave amplitudes and peak times was not significantly affected.

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