The results in
Figures 5A and
5C indicate that the rising phase of the photopic ERG response was delayed by RGS11 deficiency, a deficit that was accentuated by the addition of the RGS7 mutation. It is unclear from
Figure 5A whether the ERG changes in the RGS11
−/− and RGS7
Δ/Δ/RGS11
−/− mice resulted from a decrease in the slope of the rising phase and/or a delay in the onset of the rising phase of the ERG. To investigate, we calculated the maximum rate of increase (i.e., maximum slope) of the photopic ERG from the derivative of the filtered response (see the Methods section).
Figure 5D shows mean ERG derivatives for two flash intensities. The peak of the derivative function defines the maximum slope of the rising phase of the ERG response. Overall, maximum slopes were not significantly different between the ERGs of the WT and mutant mice (
Fig 5E).
Figure 5F shows the latency to reach the maximum slope plotted as a function of flash intensity. Responses of both the RGS11
−/− and RGS7
Δ/Δ/RGS11
−/− mice were clearly delayed relative to those of the WT and RGS7
Δ/Δ mice. The magnitudes of the delays were relatively constant across flash intensities with the RGS11
−/− responses delayed on average (±SE) by 4.0 ± 0.2 ms and the RGS7
Δ/Δ/RGS11
−/− responses by 7.7 ± 0.2 ms relative to those of WT mice. Groups were statistically compared at the intensities indicated by the vertical lines in
Figure 5F. The RGS11
−/− and RGS7
Δ/Δ/RGS11
−/− responses were significantly delayed (
P < 0.001) relative to the WT and RGS7
Δ/Δ responses. At the higher intensity, the RGS7
Δ/Δ/RGS11
−/− responses were also significantly delayed (
P < 0.05) relative to the RGS11
−/− responses, demonstrating that RGS7 contributes to the ON-BPC response. The results from
Figures 5C–F suggest that the delayed rising phase of the photopic ERGs in RGS11
−/− and RGS7
Δ/Δ/RGS11
−/− mice is primarily due to an increased latency before the onset of the response.