44
the electrical stimuli (figure 3.7), and had a lower cutoff frequency. This suggests that the
components of this decay are due to the limited frequency response of the photocurrent,
and not the low-pass filter of the cell membrane. Cones saw a similar increase in low fre-
quency components with HCN channels blocked, although the light intensities to achieve
this affect were greater (5.46 ∙ 10^2 lux). The voltage falloff at 1 Hz was less sharp than in
rods, which is consistent with the faster kinetics of the cone photocurrent. Both rods and
cones showed an increase in low frequency amplitudes, and greater frequency dependent
decay with HCN block. Comparing the normal light frequency responses to those with
HCN channels blocked demonstrates that HCN channels act as a compensator that cancels
out the frequency-dependent decay in the light response over the range from 0 to 1 Hz. On
a cellular level, slowly changing hyperpolarizing stimuli turn on HCN channels, which turn
on and shunt the original stimulus, reducing its intensity.
3.3.5 HCN contribution to GWN estimated kernel (impulse response)
The impulse responses of rod and cone photoreceptors were estimated using gaussian-white-
noise (GWN) light stimuli according to the Lee-Schetzen method [80]. A GWN stimulus
approximates physiologic conditions for photoreceptors, with luminance in a visual scene
fluctuating around a steady mean, as opposed to a flash stimulus, which measures the dark-
adapted response to a single flash impulse. Briefly, the impulse response demonstrates the
duration of time necessary for a system to respond to an infinitely brief stimulus. At dim
light intensities (1.19 ∙ 10^2 lux), the impulse response of a normal rod is shown to increase
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