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assumed to determine the speed of recovery of the rhodopsin pigment
in the dark and, hence, the speed of the dark-adaptation process.
Consequently, he suggested that dark adaptation would proceed most
slowly when all rhodopsin molecules had been bleached.
The hypothesis that the photopigment rhodopsin could account
for the sensitivity difference between rods and cones was apparently
first unequivocally put forward by Parinaud ( 1885 ). He had found that
'hèmèralopie' reduced the sensitivity of the eye markedly and attrib-
uted this sensitivity reduction to the non-functioning of rhodopsin.
In fact, he held that only the rod receptors had the ability to increase
their sensitivity during dark adaptation and that the amount of
rhodopsin determined the variation in sensitivity of the eye both
during light and dark adaptation. He found confirming evidence in
that the central fovea, which contained only cones, did not function
in night vision, and that the photochromatic interval (the intensity
interval between absolute light and chromatic thresholds) was nearly
absent in the central fovea.
The final conclusive proof that the photopigment rhodopsin
in the rods was responsible for night vision was given a few years
later by König ( 1894 ) who showed that the spectral absorption of
rhodopsin in humans closely coincided with the scotopic spectral
visibility curve.
However, the suggestion of Parinaud that only the rods had
the capacity to increase their sensitivity during dark adaptation was
found to be wrong. Thus, Loeser ( 1904 ) convincingly demonstrated
that the cones also had the ability to adapt to darkness. In fact,
following strong bleaches he found that cones could improve their
sensitivity by more than 1 log unit during the first few minutes of
dark adaptation.
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