46
in magnitude and duration when HCN channels are blocked with ZD 7288 (figure 3.9 Al).
However, at brighter light intensities, the impulse response was relatively unchanged by
blocking HCN channels (figure 3.9 A2). By shortening the duration of the impulse response,
HCN channels reduce the amount of time necessary for rods to encode an impulse of infor-
mation in dim conditions. The lack of effect at brighter intensities could be due to saturation
of the rod light response. At a higher mean luminance level, impulses of light or darkness
on top of the mean luminance are not able to cause significant changes in the rod voltage
response, and as a result, these smaller fluctuations do not cause significant changes in HCN
channel activation. Figure 3.8 shows that HCN blockade does not affect the light impulse
response much at brighter mean luminances. HCN channels appear to be most effective for
the normal operating state of rod photoreceptors—under dim light.
On the other hand, in cones, the impulse response to dim light (2.46 ∙ 10^2 lux) was
seen to be relatively unaffected by blocking HCN channels (figure 3.9 Bl). This is likely due
to minimal HCN activation by cones at dim light intensities. At brighter light intensities
(5.46 ■ IO-2 lux), HCN block caused an increase in the magnitude and duration of the im-
pulse response, similar to the change seen in rods at low light intensities (figure 3.9 B2). This
implies that under brighter light, the normal operating condition for cones, HCN channels
are functioning optimally, and help to reduce the amount of time needed to encode an im-
pulse of information. The differential effect of dim vs bright light on the function of HCN
channels in rod and cone photoreceptors coincides with the normal operating characteristic
of these two cell types. Rods, which are sensitive to small changes in light intensity in dim
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