| |
Dark adaptation
Dark Adaptation: Photopic and Scotopic Thresholds
Recovery of sensitivity in the photopic and scotopic systems during the course of dark adaptation can be illustrated by the solid-line curve in Figure 54.1. This classic curve (e.g., Hecht et al., 1937) is obtained by first exposing the eye to a large, uniform, bright light and then plunging it into total darkness. The threshold—the intensity of light just needed to detect a small, brief test flash—is determined at regular intervals as dark adaptation progresses. The threshold curve divides Figure 54.1 into two regions: test flash intensities below the threshold are invisible, while those above it are visible. The curve has two segments or limbs. In the first 2 minutes, detection thresholds drop rapidly and then taper off at the absolute photopic threshold. After a few more minutes the curve again drops, somewhat less rapidly, and reaches a final level, the absolute scotopic threshold, after about 45 minutes.
Figure 54.1..
Solid line: Thresholds for brief blue or green parafoveal test flashes, expressed in logarithmic units relative to the scotopic absolute threshold. Abscissae are minutes in the dark following exposure to a bright, uniform adapting light. Dotted line: foveal flashes.
The progressive drops in threshold correspond to increases in visual sensitivity, first of the photopic system and then of the scotopic system. The change from one system to the other is called the rod-cone break, since in the duplicity theory scotopic vision is mediated exclusively by the rod photoreceptors and photopic vision by the three types of cone photoreceptors. Just-visible blue or green test lights appear colored if flashed before the break, indicating cone function, and colorless after it, indicating rod function. The ordinate in Figure 54.1 is in logarithmic units, so the threshold data illustrate a recovery in sensitivity on the order of 4 log units (or 10,000 to 1), of which the first log unit is due to recovery of cones, and the final three log units, of rods.
Figure 54.1 illustrates a dark adaptation curve produced by a blue or green test flash delivered to a peripheral retinal position where both rods and cones are numerous. When the dark adaptation curve is measured with long-wavelength (red) test flashes which are invisible to the rods, or with test flashes restricted to the rod-free foveal region, there is only a photopic limb, as indicated by the dashed line. All test flashes whose intensities fall between the dotted and the continuous line are detected by the rods alone. These curves simply illustrate duplicity. An enormously important practical application is due to Miles (1943), who first put on red goggles a half hour before night duty so that he could keep on reading (with his cones) while allowing his rods to regenerate; later, while on night duty, if he needed to go into a lit area, he put the goggles back on and preserved most of his dark adaptation.
The Purkinje Shift
Relative brightness also changes at the rod-cone break. This change is called the Purkinje shift, after the Czech physician who noticed that differently hued flowers of similar brightness in daylight may differ in brightness in twilight. The shift can be quantified as a change in the peak spectral sensitivity of the eye from yellow-green or 555 nm (the photopic peak) before the break to blue-green or 507 nm (the scotopic maximum—the peak sensitivity of rhodopsin, the rod-photosensitive pigment) after it. While in daylight equally reflective yellow and blue-green flowers will seem about equally bright, as their spectral centroids straddle the photopic peak, in twilight the yellow flower will appear much dimmer, as its spectral centroid is far from the scotopic peak. In general, differently colored stimuli whose brightnesses match in daytime will differ in twilight unless the stimuli are restricted to the rod-free fovea (von Kries and Nagel, 1900). Fully appreciating the Purkinje shift frees the student from both the stimulus error—the assumption that a visual experience necessarily denotes a true state of affairs in nature—and the (often implicit) idealist belief that perception is purely mental, as the brightness matches are biophysically determined.
Adaptive Independence
The two limbs of the dark adaptation curves are not locked into place. They can be translated vertically (on a logarithmic scale of intensity) by altering the preadaptation light in wavelength composition or in intensity and by altering the test flash in wavelength, size, location on the retina, or duration (Barlow, 1972). These are all factors governing visual sensitivity; e.g., enlarging the test lowers the threshold due to summation in the retina. However, if the two limbs do appear, their time courses will be as shown. This invariance occurs because each class of photoreceptor recovers independently of the adaptive states of the other class of photoreceptor. Indeed, if the subject is a rod monochromat (i.e., has no photopic function), his dark adaptation proceeds along the same time course as that of the rods of the normal subject (Rushton, 1981; Sharpe and Norby, 1990).
The principle of adaptive independence also holds in photopic vision to the extent that each class of cones recovers along a time course independent of the other classes of cones. Such independence may be explained by the electrical and chemical isolation of (mammalian) photoreceptors from each other. An exception to independence occurs at high light levels when electrical synapses between cones of different classes permit weak interactions. However, adaptation can occur not only in the cones but also at subsequent sites in the visual system, and recovery of these sites may also affect thresholds during dark adaptation. Thus threshold measurements may or may not demonstrate adaptive independence, depending on whether these subsequent sites of adaptation are involved. To illustrate, there are chromatically sensitive sites in the retina which receive opponent inputs from different cone classes (L versus M or S versus L and M). Adaptation of such sites can generate gross violations of the normal course of dark adaptation (see “Anomalies of Photopic Dark Adaptation” below).
Bleaching and Recovery from Bleaching
Vision starts with the capture of individual quanta of light by photopigment molecules located in the photoreceptors. Quantal captures bleach the photopigment molecule, which becomes transparent to light for some time after capture; only unbleached photopigment molecules are active—can respond to light. Bleaching plays a major role in regulating the sensitivity of the cones at the very highest light levels (10,000 cd/m2 or above). After prolonged light adaptation to very high levels, even further increases in light intensity are balanced by decreases in the active cone photopigment, so the cones signal a steady level of light instead of an increase. This protective function of bleaching implies that the photopic system is not driven into saturation by intense sunlight. However, to restore sensitivity in the dark requires the photopigment to regenerate (recover from the bleached state). Regeneration is not instantaneous; rather, as dark adaptation continues, progressively more of the photopigment molecules regenerate and become actively available for capturing light.
The recovery of threshold with time in the dark following a bleach has been studied in great detail. Figure 54.2 shows 10 such recovery curves from 10 different light adaptations (from Hollins and Alpern, 1973). More intense adaptations (the rightward march of the curves) bleached more and more photopigment. The curves show how cone photopigment recovers exponentially during the first 5 minutes in the dark from the initial bleach. The close fit of the log thresholds (symbols) to the pigment recovery curves shows that as the fraction of active pigment molecules increases in the dark, log threshold falls toward the absolute threshold. It is important that this agreement is obtained only when thresholds are plotted on a logarithmic scale.
Figure 54.2..
Symbols show recovery of L-cone-mediated foveal thresholds after 1 minute of light adaptation to bleaching lights. From right (open circles) to left (filled inverted triangles), 100%, 80%, 70%, 60%, 59%, 40%, 30%, 20%, 15%, and 10% of photopigment was bleached. Data are shifted to the right for clarity; each time origin is indicated by a bar above. Curves show how cone photopigment recovers from the level determined by the light adaptation for the first 5 minutes in the dark. Agreement between data and curves shows that log threshold (not threshold per se) is related to the amount of photopigment. (After Hollins and Alpern, 1973.)
It might seem that recovery from bleaching accounts for the recovery of threshold simply by increasing the number of photopigment molecules available to catch quanta. However, this is not so. A 50% bleach, for example, removes only half of the photopigment molecules available for catching quanta of light, but it raises thresholds by 100 times, not by 2 (open squares, middle of Fig. 54.2; note the log10 scale for thresholds). Even after a mild bleach, when 90% of the cone photopigment is active, the threshold is still 10 times the cone absolute threshold (inverted triangles, far left of Fig. 54.2), not 1.1 times it. Similarly, rod thresholds can be 100 times the rod absolute threshold when 90% of the rhodopsin photopigment has recovered (Hecht et al., 1937). True, thresholds recover along the photopigment trajectory, at least after the stronger adaptations (Fig. 54.2), but this cannot be explained by the mere increase in the number of photopigment molecules available to catch quanta.
Photoproducts of Bleaching: the Veiling Effect
One explanation of data like those in Figure 54.2 is that photoproducts of bleaching remain in the receptors when the eye is in darkness, and these photoproducts act as an equivalent light which veils the incoming test flash and thus elevates the threshold. It is the progressive removal of these photoproducts which, by rending the veil (so to speak), reduces the equivalent to light and permits the threshold to recover. The term veil is used because thresholds for test flashes can also be elevated by glare sources—e.g., bright lights such as automobile headlamps, which, placed in the periphery of the visual field, generate a veil of real light across the eye. Stiles and Crawford (1937) showed psychophysically that, following bleaches, the human visual system behaves as though it were experiencing a veil equivalent to a real glaring light.
This metaphor may seem strained because, unlike the real light with which it can be equated, equivalent light is invisible. One typically sees a black field, not a visible afterimage, during the course of dark adaptation. However, real lights also become invisible if, like the equivalent light, they are retinally stabilized. Only if the edges of a field of light move on the retina is the retina able to signal its presence to the brain. Therefore, the assumption that an invisible equivalent to real light acts to raise the threshold is not as farfetched as it may appear.
The notion that photoproducts of bleaching account in part for recovery in the dark is tenable if the time course of their recovery matches up with the psychophysics. The next section discusses this point in detail and can be skipped without loss of continuity.
Photoproducts of Bleaching: Theory
A detailed theory of bleaching and equivalent light has been developed by Lamb and colleagues for scotopic dark adaptation in the toad retina (summarized in Leibrock et al., 1998, and Chapter 16, this volume). A physical basis for equivalent light is postulated to exist in the rod. The rod rhodopsin molecule, Rh, is activated to the form Rh* either by photon absorption—indicating light—or as a result of spontaneous thermal isomerization—a source of thermal noise that the visual system must somehow ignore (Barlow, 1988). Rh*, the virgin metarhodopsin II, or MII, then activates the G-protein cascade by catalyzing the conversion of inactive G to its active form, G*. Rh* is rapidly inactivated to the form MII-P-Arr, which is thought to be the main photoproduct generating the equivalent light.
MII-P-Arr is thought to act via two mechanisms which generate rather different forms of equivalent light. First, a molecule of MII-P-Arr will very occasionally revert to Rh*. This mechanism will generate spurious events (noise) which are identical to real photon captures, thus producing false alarms—reports of light when none exists. Second, the ability of MII to activate the G-protein cascade is not totally eliminated by phosphorylation and arrestin binding; instead, MII-P-Arr can act directly on the phototransduction mechanism. The effects of this second mechanism will also resemble light in leading to steady activation of the cascade, although with less extreme fluctuations. At the start of dark adaptation, the scotopic threshold is controlled primarily by the second mechanism, which initially generates far more equivalent light than the first. The second mechanism recovers relatively quickly, however, following the decay of MII-P-Arr (the human time constant of 2 minutes for this process agrees with that of the toad rod after correction for the toad's lower body temperature). This accounts for the relatively fast initial drop of threshold following the rod-cone break in Figure 54.1. The subsequent slow recovery of scotopic vision to absolute threshold, extending out to 45 minutes, is due to a slow reduction in the frequency of the photon-like noise events contributed by the first mechanism.
Rod-Cone Interactions during Dark Adaptation
The distinctness of the rod-cone break seen at threshold in Figure 54.1 does not imply that vision is mediated by one or the other type of receptor; indeed, above threshold, both types of receptor may respond to a test flash. Whether this occurs depends both on the level of the original light adaptation and on the intensity of the test flash. After adaptation to bright lights, the rods or rod pathways will saturate, and rods will not contribute to vision until some time has passed in the dark. When recovered, however, unsaturated rods can contribute to the visibility of test flashes presented to the cones. One example in which rods and cones contribute to flicker perception is presented in Chapter 55 (Fig. 55.5). Another example is the progressive desaturation (apparent whitening) of colored test flashes which occurs as the rods increasingly recover in the dark. Judging the degree of saturation is not easy, but it is easy (with practice) to adjust the intensity of a test flash until it appears just visibly colored (the hue specific threshold). As dark adaptation progresses, the specific threshold actually rises (as shown for a green test flash in Fig. 54.3 by open circles), contrary to the fall in detection threshold seen in Figure 54.1 and repeated in Figure 54.3 (filed circles), presumably to overcome the increasing achromatic response elicited from the recovering rods. Lie (1963) showed that this effect held for blue, green, yellow, and orange test flashes but not for red flashes, whose wavelengths were long enough to escape detection by the rods.
Figure 54.3..
The specific threshold for just noticing hue (open circles) compared to the threshold for detection (filled circles), for a green test, during 30 minutes of dark adaptation. Flashes were 6 degrees parafoveal. The observer initially adapted to a large white 4000 mL field. (After Lie, 1963.)
Retinal or Cortical Origins of So-Called Rod-Cone Interactions
Although the Lie effect, and others like it, are called rod-cone interactions, no direct interaction is necessarily implied. Rod signals must piggyback on those of cones (directly via electrical gap junctions or indirectly via AII amacrine cells) to access the ganglion cell axons which transmit signals to the mid-brain, from which they travel to the cortex. Ganglion cells which signal hue, whose inputs come entirely from cones, are distinct from ganglion cells which signal luminance, whose inputs come from both rods and cones. It is conceivable for cortical interactions between luminance-encoding and hue-encoding cells to give the appearance of rod-cone interactions (see Chapter 55).
It is sometimes possible to separate cortical from retinal interactions by comparing monocular and dichoptic stimulations. An example relevant to dark adaptation is provided by the interocular light adaptation effect (Landsford and Baker, 1969), in which the rod-cone break occurs 3 minutes later after light adaptation of the test eye alone than after an equal light adaptation of both eyes. This effect is illustrated in Figure 54.4, taken from Prestrude et al. (1978), who also showed that the Lie effect was similarly delayed. The difference in thresholds is considerable, a factor of about 5 times after 15 minutes in the dark; it is still not known what causes the effect or why it is so large, but its interocular origin implies that it occurs cortically rather than in the retina.
Figure 54.4..
The interocular light adaptation effect. Test flashes were green and parafoveal. M, position of the rod-cone break following monocular adaptation to a bleaching light; D, position of the break following dichoptic adaptation to the same light in the test eye and an overlapping but dimmer light in the nontest eye. The delay (from D to M) is 3 minutes. (From Prestrude et al., 1978.)
Even the scotopic absolute threshold is affected by cortical interactions: one-eyed people have slightly better night vision than normals, and bleaching the cones of the nontest eye of a two-eyed person will slightly lower the scotopic absolute threshold (by
2
) in the other eye for up to 10 minutes (Reeves et al., 1986). This can be explained if dark light from cones in a dark-adapted eye contributes noise to a central detection stage used to detect rod signals from either eye, assuming that enucleation or bleaching acts to improve vision by halving the noise at the detection stage.
Anomalies of Photopic Dark Adaptation
Photopic dark adaptation curve do not necessarily follow the first, descending, limb of Figure 54.1 (Stiles, 1949). Indeed, some violations of the rapid recovery are dramatic enough to have been termed anomalies of dark adaptation (Mollon, 1982).
The classic recovery curve shown in Figure 54.1 does occur if the observer attempts to detect the test flash, where detection can be based on any visual sensation at all. For example, detection of a long-duration red test flash may be based on its hue or its luminance; on a temporal transient at stimulus onset or a sustained spatial comparison between the test and the field; or even on an afterimage left behind when the flash is over. As detection is defined here, the choice is entirely up to the subject (and is generally not known by the experimenter).
However, the dark adaptation experiment can be repeated with test flashes whose thresholds are determined by sensitivity to one or another particular sensation. There are several methods for isolating specific sensations, which involve the choice of test stimulus or an instruction to the subject as to what property of the test to report. An example of the latter, already mentioned, is the specific threshold for just noticing a stimulus hue, which in fact rises after several minutes of dark adaptation. It is better, if possible, to design the test stimulus so as to elicit only one sensation, which removes the ambiguities inherent in the instruction. Thresholds for such special stimuli show that for some (but not all) light adaptations, the sensitivities of the photopic pathways which respond to fast luminance flicker (Reeves and Wu, 1997) and to hue (Mollon, 1982) may be abruptly reduced at the start of dark adaptation. Sensitivities may be reduced (and hence thresholds elevated) by a factor of 10 or 100, depending on conditions, so the anomalies are not minor. After such an abrupt desensitization, sensitivity typically recovers fairly slowly.
Illustrative data showing the loss of sensitivity for blue test flashes after exposure to yellow-adapting fields (termed transient tritanopia, meaning short-term blue blindness) were obtained in an extensive exploration by Augenstein and Pugh (1976). Whereas the green flash thresholds showed normal light adaptation (filled circles, left half of the plot of Fig. 54.5) and recovery (filled circles, right half), the blue test flashes first rose at light onset, then stabilized close to absolute threshold, and then rose again at light offset before eventually recovering (open circles). The blue test flash thresholds were special (in the above sense) because the blue tests were detected by S cones, which elicit only hue sensations.
Figure 54.5..
Thresholds for test flashes exposed during 5 minutes of light adaptation to a bright but nonbleaching yellow field (left half of the plot) and following offset of the field (right half of the plot). All thresholds are plotted in log units relative to absolute threshold. Light adaptation has a pronounced and continuous effect on green test flash thresholds, as the yellow field desensitizes M cones (closed circles, upper left). In contrast, light adaptation produced a smaller and temporary effect on blue test flash thresholds (open circles, lower left); this was necessarily mediated by an opponent site, as S cones were not adapted by the yellow field. The dark adaptation curves show normal recovery for the green test flash (closed symbols, lower right) but a surprising rise in threshold for the blue flash (open circles, middle right), illustrating rebound. (After Augenstein and Pugh, 1976.)
The next section (which may be skipped without loss of continuity) offers Pugh and Mollon's (1979) theory of the roller-coaster ride of the blue flash thresholds. The theory is of a black box nature, as this dramatic violation of the usual course of adaptation has not yet been explained at the physiological level. However, as it occurs only when test and adaptation fields are presented to the same eye, it is very likely a purely retinal effect—indeed, transient tritanopia was seen in the electroretinogram by Valeton and Van Norren (1979).
Hue-Pathway Anomalies: Theory
Pugh and Mollon (1979) theorized that an abrupt desensitization (followed by slow recovery) in early dark adaptation may be caused by a transient rebound of a polarized site. This theory was developed in the case of transient blue blindness (transient tritanopia) following onset and offset of an adapting yellow field (Fig. 54.5). This case is analytically special, since with the appropriate choice of stimuli, only S cones can detect the blue test flash and only L and M cones are light adapted by the yellow field. The S-cone test flashes can only be detected by their hue because S cones contribute virtually nothing to luminance. Thus, for the S-cone pathway to be desensitized when the yellow field is turned off, the rebound must occur at an opponent site which receives antagonistic inputs from S cones (blue) versus L and M cones (yellow).
This theory correctly implies normal recovery for blue test flash thresholds after turning off a 500 nm green field, as a 500 nm field is neutral, biasing the yellow-blue pathway neither toward yellow nor toward blue (unlike longer-wavelength fields, which polarize the pathway in the yellow direction), so turning it off does not generate a rebound (data not shown).
Pugh and Mollon postulated that the yellow/blue pathway is most sensitive when it is in a neutral state (adapted to white, gray, black, or green) and least sensitive when polarized (adapted to yellow or blue). They also hypothesized that during light adaptation to a polarizing field, such as yellow, a force develops fairly slowly (∼15 second time constant) which opposes the polarizing signal and restores neutrality. Such a force works to make the yellow sensation generated by the field appear progressively whiter as light adaptation continues. Thus, at onset of the yellow field, blue test thresholds are initially driven high by the unopposed yellow polarization, but they fall progressively as the opposing force begins to neutralize the opponent site. After offset of the yellow field, the still active opposing force drives the site in the opposite (blue) direction, again making it less sensitive. The opposing force then decays with the same ∼15 second time constant. The roller-coaster blue test flash thresholds in Figure 54.5 are entirely explained by a resistor-capacitor-circuit formulation of this idea (smooth curve).
This explanation does not refer to the appearance of the visual field once the yellow light has been turned off. One might think that after turning off of the field, the still active opposing force would generate a vivid blue afterimage, perhaps accounting for the difficulty in detecting blue flashes. However, subjects report seeing black, not blue. Nevertheless, if the yellow field is reduced in intensity by 10 times rather than being turned off, subjects do report a vivid blue afterimage (Reeves, 1983). Moreover, desensitization still occurs, is almost as large, and follows the same slow recovery process as when the eye is plunged into total darkness. Perhaps there always is a blue afterimage, which is kept visible (to the cortex) when the field is dimmed because the field constantly moves on the retina due to inescapable small eye movements but which fades to blackness when the field is off and there is no retinal motion to reevoke it.
The Pugh-Mollon theory is the best one available, but in its RC form it does not account for the abolition of transient tritanopia with light adaptation to 0.5 Hz flickering yellow fields (Reeves, 1983). Nor does it account for the reduction in transient tritanopia, and the different spectral sensitivity of the residual effect, found when S cone decremental test flashes are employed instead of S cone incremental test flashes (Eskew and McLellan, 2000). These effects require postulating additional stages of integration and distinct S-ON and S-OFF opponently coded pathways.
A Red/Green Anomaly
The Pugh-Mollon theory, originally developed for the S-cone pathway, can also be applied to the red/green process. Sensitivity to red and green tests detected by the red/green opponent process is reduced at the start of dark adaptation if the light adaptation has been polarizing (in this case, red and green fields; white, black, and yellow are neutral). An analytical experiment in this case is tricky, because L and M cones also contribute to luminance, and luminance sensitivity recovers, permitting detection thresholds for red, yellow, or green test flashes to follow the descending photopic limb in Figure 54.1. However, it is possible to isolate the red/green hue pathway using hue flicker generated by alternating 580 nm and 640 nm test lights, whose hues are easily distinguishable, at rates of 4 to 6 Hz which are optimally visible for the hue pathway (Reeves, 1983). The lights were equated in luminance throughout dark adaptation to eliminate luminance flicker as a cue. Figure 54.6 shows the resulting hue (visible flicker) and detection thresholds as a function of time in the dark following offset of a 626 nm (polarizing) field.
Figure 54.6..
Thresholds for hue flicker and detection, plotted in logarithmic units relative to photopic absolute threshold (T0). The upper curves show the entire time course of recovery; the lower panel shows just the first 2 seconds. Open circles show the hue flicker thresholds; open squares, thresholds for detection.
Figure 54.6 (top) shows that thresholds for reporting hue flicker lie above those for detection throughout the period of dark adaptation. This effect is hard to see at the start, when the thresholds fall on top of each other, so the first 2 seconds have been stretched out in the lower panel for clarity. The first two data points in the lower panel (at the far left) indicate the two thresholds on the steady light-adapting field just before it was turned off. They are close, showing that almost as soon as one can detect the test at all, one can see it flicker. Only after the field is turned off do the thresholds diverge. The explanation in Pugh-Mollon terms is that the offset of the 626 nm (red) field produced a rebound in the red/green hue sensitive pathway. This rebound raised the hue flicker thresholds but did not affect the detections, which were based on luminance transients at test onset and offset rather than on seeing hue (Fig. 54.6). Indeed, after turning off a yellow field, which is neutral in the red/green pathway, both types of threshold recover equally (Reeves, 1983). There are other close correspondences between the yellow/blue and red/green pathways; in both cases there are no rebounds after offsets of bleaching fields (Mollon, 1982), and adapting to slowly flickering polarizing fields does not produce rebounds (Reeves, 1983). Since no gross divergences have since been discovered, the upshot appears to be that the dark adaptation of both yellow/blue and red/green pathways follows the same laws.
Luminance Anomalies
A transient tritanopia–like effect termed transient lumanopia has recently been discovered in the luminance pathway. Sensitivity to rapidly flickering white light (>12 Hz) may be reduced abruptly and dramatically, by up to 60 times, at the start of dark adaptation (Reeves and Wu, 1997). When this happens, sensitivity takes many seconds to start recovering. Although this might suggest a rebound in an opponently coded black/white pathway, analogous to the opponent pathway assumed by Pugh and Mollon (1979) to explain transient tritanopia, fast flicker in fact stimulates a nonopponent or additive luminance-sensitive channel. (Slower flickers stimulate other luminance-sensitive channels.) The additive channel can be approximated by a filter which is maximally sensitive to lower frequencies and progressively attenuates higher ones. The frequency at which attenuation is 50% (i.e., sensitivity is one-half of maximum) provides a benchmark called the corner frequency. Reeves and Wu postulated that the corner frequency is abruptly lowered at the start of dark adaptation. For example, immediately after turning off a 400 Td white adapting field, the corner frequency drops from 20 Hz (the light-adapted level) to 10 Hz. The dramatic size of the lumanopia effect occurs because the luminance filter attenuates very rapidly, so that 18 Hz flicker, which is easily visible in the light, is attenuated 60-fold when the corner frequency drops to 10 Hz. According to this postulate, any test stimulus, even as a single flash, that can be detected via a relatively slow (<10 Hz) luminance-sensitive channel would not suffer lumanopia but rather would exhibit classical dark adaptation.
Summary of Dark Adaptation
The classic recovery of photopic vision seen in Figures 54.1 and 54.2 is an important characteristic of the visual system and illustrates how adaptation occurs over a large range of light levels. Psychophysically it can be measured if the test flash stimulates a luminance channel sensitive to low temporal frequency components (these are present in a long-duration test flash or a flash which flickers at a low rate). Recovery in this channel may follow the time course of recovery of the cones themselves if veiling is taken into consideration. However, other channels, sensitive to hue or fast flicker, are typically desensitized at the start of dark adaptation. The physiological underpinnings for these large psychophysical desensitization effects are not known in detail, but in the case of hue they probably involve desensitization and recovery of retinal sites at which inputs from various classes of cones are opponent. The recovery of scotopic vision seen in the rod limb of Figure 54.1 is not subject to such anomalies and can be explained in terms of recovery of physiological mechanisms which create equivalent light.
| |
