We have employed two paradigms to investigate the mechanisms of contrast gain control in cat striate cortex. In the first paradigm, optimal drifting gratings were presented in three consecutive periods. The contrast was near threshold in the first and third periods and accompanied by iontophoretic pulses of glutamate or glutamate receptor (GluR) agonists. The contrast was set to evoke a higher firing rate in the second period. Although both visual and iontophoretic conditions were identical in the first and third periods, responses to glutamate, N-methyl-D-aspartic acid (NMDA), and (1S, 3R)-1-Aminocyclopentane-1, 3-dicarboxylic acid (ACPD) were reduced following the adapting interval. (S)-α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) responses were not reduced. Administration of ionotropic GluR antagonists did not affect adaptation to the high-contrast grating. The metabotropic GluR antagonist (±)-α-Methyl-4-carboxyphenylglycine (MCPG), which acts at presynaptic glutamate autoreceptors, decreased the degree of adaptation exhibited by striate cells. In a second paradigm, contrast response functions (CRFs) were obtained at various adapting contrasts and least-squares fits to a hyperbolic ratio equation generated for each adapting level. Similar to previous reports, DL-2-amino-5-phosphonovaleric acid (APV) reduced the slope of the CRF and increased the responsiveness of the cells but did not affect the semisaturation constant, σ, or the exponent of the CRF, n. Only MCPG significantly altered the distribution of σ and n for 19 cells. The effect on α suggests that this drug can interfere with the cell's ability to shift its operating point to match the adapting contrast. These results suggest the involvement of a presynaptic mechanism for contrast adaptation. The decrease in neuronal responsiveness immediately following the high-contrast period may reflect an additional, postsynaptic effect in which there is a decrease in the NMDA-mediated component of the visual response.

An aftereffects paradigm was used to behaviorally measure contrast sensitivity of cats to gratings of three different test spatial frequencies after adaptation to gratings of various spatial frequencies, contrasts, and durations. Post-adaptation reductions in sensitivity occurred even after short periods of adaptation (<7 s) and could be as large as 1.0 log unit under some conditions. The magnitude of the adaptation effect varied monotonically with (1) adaptation grating contrast, (2) duration, and (3) the contrast sensitivity for the test grating. Average half-width (at half-height) of the spatial-frequency tuning curves constructed from the data was 1.4 octaves, and was not dependent upon the level of adaptation or the spatial frequency of the test grating. Post-adaptation psychometric functions of the cats showed reduced slopes and maxima suggesting that, unlike humans, in cats apparent contrast grows more slowly with increases in physical contrast after contrast adaptation. All of the characteristics observed are in excellent agreement with electrophysiologically measured properties of neurons in striate cortex of cats. In addition, there was a remarkable similarity of the cat tuning functions, both in shape and bandpass, to those measured in man with a similar paradigm suggesting that (1) the two visual systems are sufficiently similar to make the cat a useful spatial vision model and (2) there is a common functional plan to all mammalian visual systems despite significant anatomical differences between species.

We recorded visual evoked potentials in response to square-wave contrast-reversal checkerboards undergoing a transition in the mean contrast level. Checkerboards were modulated at 4.22 Hz (8.45-Hz reversal rate). After each set of 16 cycles of reversals, stimulus contrast abruptly switched between a “high” contrast level (0.06 to 1.0) to a “low” contrast level (0.03 to 0.5). Higher contrasts attenuated responses to lower contrasts by up to a factor of 2 during the period immediately following the contrast change. Contrast-response functions derived from the initial second following a conditioning contrast shifted by a factor of 2–4 along the contrast axis. For low-contrast stimuli, response phase was an advancing function of the contrast level in the immediately preceding second. For high-contrast stimuli, response phase was independent of the prior contrast history. Steady stimulation for periods as long as 1 min produced only minor effects on response amplitude, and no detectable effects on response phase. These observations delineate the dynamics of a contrast gain control in human vision.

We used color contrast adaptation to examine the chromatic and contrast selectivity of central color mechanisms. Adaptation to a field whose color varies along a single axis of color space induces a selective loss in sensitivity to the adapting axis. The resulting changes in color appearance are consistent with mechanisms formed by different linear combinations of the cone signals. We asked whether the visual system could also adjust to higher-order variations in the adapting stimulus, by adapting observers to interleaved variations along both the L versus M and the S versus LM cardinal axes. The perceived hue of test stimuli was then measured with an asymmetric matching task. Frequency analysis of the hue shifts revealed weak but systematic hue rotations away from each cardinal axis and toward the diagonal intermediate axes. Such shifts could arise if the adapted channels include mechanisms with narrow chromatic selectivity, as some physiological recordings suggest, but could also reflect how adaptation alters the contrast response function. In either case they imply the presence of more than two mechanisms within the chromatic plane. In a second set of measurements, we adapted to either the L versus M or the S versus LM axis alone and tested whether the changes in hue could be accounted for by changes in relative contrast along the two axes. For high contrasts the hue biases are larger than the contrast changes predict. This dissociation implies that the contrast and hue changes are not carried by a common underlying signal, and could arise if the contrast along a single color direction is encoded by more than one mechanism with different contrast sensitivities or if different subsets of channels encode contrast and hue. Such variations in contrast sensitivity are also consistent with physiological recordings of cortical neurons.

Contrast adaptation occurs in both the retina and the cortex. Defining its spatial dependence is crucial for understanding its potential roles. We thus asked to what degree contrast adaptation depends on spatial frequency, including cross-adaptation. Measuring the pattern electroretinogram (PERG) and the visual evoked potential (VEP) allowed separating retinal and cortical contributions. In ten subjects we recorded simultaneous PERGs and VEPs. Test stimuli were sinusoidal gratings of 98% contrast with spatial frequencies of 0.5 or 5.0 cpd, phase reversing at 17 reversals/s. Adaptation was controlled by prolonged presentation of these test stimuli or homogenous gray fields of the same luminance. When adaptation and test frequency were identical, we observed significant contrast adaptation only at 5 cpd: an amplitude reduction in the PERG (−22%) and VEP (−58%), and an effective reduction of latency in the PERG (−0.95 ms). When adapting at 5 cpd and testing at 0.5 cpd, the opposite effect was observed: enhancement of VEP amplitude by +26% and increase in effective PERG latency by +1.35 ms. When adapting at 0.5 cpd and testing at 5 cpd, there was no significant amplitude change in PERG and VEP, but a small effective PERG latency increase of +0.65 ms. The 0.5-cpd channel was not adapted by spatial frequencies of 0.5 cpd. The adaptability of the 5-cpd channel may mediate improved detail recognition after prolonged blur. The existence of both adaptable and nonadaptable mechanisms in the retina allows for the possibility that by comparing the adaptational state of spatial-frequency channels the retina can discern between overall low contrast and defocus in emmetropization control.

Previous studies of human contrast adaptation employing visually evoked potentials (VEP) have revealed contradictory results, namely, either a reduction or an enhancement in VEP amplitude. In a cross-adaptation experiment, we explored the possibility that differences in the temporal frequency of adapting and test patterns played a role. Phase-reversing checkerboard stimuli [1-deg check size, temporal frequency 8.5 or 17 reversals per second (rps)] served as adaptation and test pattern with contrasts of 0 or 97%. In 13 subjects, we recorded both retinal (PERG) and cortical (VEP) steady-state responses simultaneously. In a balanced block design, all four combinations of the temporal adaptation and test frequencies were employed. Contrast adaptation reduced the PERG amplitude by about 20% in every temporal condition (P < 0.001). The VEP amplitude was strongly affected by adaptation, but the effect differed in magnitude and sign depending on condition: With identical adaptation and test frequency, amplitude was reduced by 15% (P = 0.07) at 8.5 rps and by 38% at 17 rps (P < 0.05). Adapting at 8.5 rps and testing at 17 rps had a tiny (14%) insignificant effect, whereas adapting at 17 rps and testing at 8.5 rps revealed an amplitude enhancement of 27% (P < 0.05). These strong temporal cross-adaptation effects (in the VEP, but not in the PERG) suggest that the adaptable cortical mechanisms (gain control) can be narrowly tuned in their temporal properties. A sizable adaptation effect can even change its sign when varying the temporal frequency by a factor of two. This finding resolves contradictions between previous VEP adaptation studies and reconciles them with psychophysical findings.