VISUAL ADAPTATION AND RETINAL GAIN CONTROLS 287

size (Biersdorf et al., 1965). This experiment
indicates that the gain of the retina is affected at
the same light levels as the visual threshold for large
targets. A further question one might raise is, where
in the retina is the site of this gain change? Much
of the physiological work we present below was
motivated by this question. Prior to the
physiological investigation, this question of the site
in the retina of gain control was investigated
psychophysically and this work led to the two
concepts of gain control by pigment depletion,
which has been shown to be only a minor factor
in the control of retinal gain, and the adaptation
pool, which still motivates research.
2.1.6.3. Pigment depletion. Vertebrate visual
pigments are bleached by light into non-receptive
intermediates which must be regenerated to a
receptive state enzymatically. It was thought for
some time that visual pigment depletion, resulting
from bleaching by the background light, was the
main cause of light adaptation (Hecht, 1924). This
would put the site of adaptation right at the initial
transduction stage in vision. However, it is now
known that the pigment regenerates so quickly that
there is a rather small amount of pigment bleached
1.0
for either rods or cones over much of the visual
range of backgrounds (Rushton, 1962). This can be
seen in Figs. 15 and 16. Figure 15 is from Alpern
and Pugh (1974) and shows the fraction of human
rhodopsin, the rod pigment, bleached as a function
of a steady background. Even up to rod saturation
(5" 108 quanta(507 nm) (deg 2 s)-~) the rod pigment
has been bleached away less than 2°70, but the visual
threshold would have risen by a factor of more than
107, a discrepancy in prediction. Figure 16 shows
a similar result for human cones, from Alpern et
ai. (1971). The cone pigment has been only bleached
by half at about 104s trolands which is near the top
of the photopic range. So we can rule out pigment
depletion as playing a major role in human light
adaptation, though it has some effect on photopic
(cone-driven) sensitivity (Boynton and Whitten,
1970; Valeton and van Norren, 1983). It is
interesting that photopigment depletion began to be
doubted as an explanation of light adaptation quite
a long time ago, from experiments on increment
threshold and photopigment concentration in the
frog retina conducted by Granit et al. (1939). In
those experiments ERG thresholds were increased
by log units by backgrounds which had no

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575 n m
~ 0.4
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0.2
500 n m
10 sec W h i t e

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12 13 14 15
Log q u a n t a sec -I c m -~ o f r e t i n a at t h e c o r n e a

FIG. 15. Pigment depletion in rods caused by steady illumination. The amount of the rhodopsin in a 5 deg field located
18 deg peripheral to the fovea in the temporal retina was measured with a retinal densitometer (described in Alpern et al.,
1971 and in Alpern and Pugh, 1974)• Plotted vertically is the fractional amount of rhodopsin left in the steady state at
the background illumination plotted on the horizontal scale. The three curves are for steady lights of 500 nm, 575 nm,
and white light• The 500 and 575 nm lights were obtained with the white source and interference filters• The results to
concentrate on are the 500 nm results, since 500 nm is near the peak wavelength of absorption of rhodopsin and so will
give the greatest pigment depletion at the lowest retinal illumination. The half bleaching point for the 500 nm curve is at
about 13.2 log quanta(cm 2 s)-' which is equivalent to about 10.2 log quanta(deg2 s)-1, the more familiar unit of retinal
illumination [also equivalent to about 4.3 log (scotopic) td]. These values of quanta are referred to the cornea and do not
take into account losses in the eye. From Alpern and Pugh 0974).
PRR3-H*