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Although reduced ambient lighting (“dim” light) can cause myopia in emmetropizing chicks, it does not necessarily lead to myopic changes in emmetropizing rhesus monkeys. Because myopia is rarely spontaneous, a question remained whether dim light would hasten the progression of visually induced myopia. To determine the effects of dim light on the development of and recovery from form-deprivation myopia (FDM), seven 3-week-old infant rhesus monkeys were reared under dim light (mean ± SD = 55 ± 9 lx) with monocular diffuser spectacles until ~154 days of age, then maintained in dim light with unrestricted vision until ~337 days of age to allow for recovery. Refractive errors, corneal powers, ocular axial dimensions and sub-foveal choroidal thicknesses were measured longitudinally and compared to those obtained from form-deprived monkeys reared under typical laboratory lighting (504 ± 168 lx). Five of the seven subjects developed FDMs that were similar to those observed among their normal-light-reared counterparts. The average degree of form-deprivation-induced myopic anisometropia did not differ significantly between dim-light subjects (−3.88 ± 3.26D) and normal-light subjects (−4.45 ± 3.75D). However, three of the five dim-light subjects that developed obvious FDM failed to exhibit any signs of recovery and the two monkeys that were isometropic at the end of the treatment period manifest abnormal refractive errors during the recovery period. All refractive changes were associated with alterations in vitreous chamber elongation rates. It appears that dim light is not a strong myopiagenic stimulus by itself, but it can impair the optical regulation of refractive development in primates.

Dual-focus lenses that impose simultaneous competing myopic defocus over the entire visual field produce axial hyperopic shifts in refractive error. The purpose of this study was to characterize the effects of eccentricity on the ability of myopic defocus signals to influence central refractive development in infant monkeys. From 24 to 152 days of age, rhesus monkeys were reared with binocular, dual-focus lenses that had central, zero-powered zones surrounded by alternating concentric annular power zones of +3D and zero power. Between subject groups the diameter of the central, zero-powered zone was varied from 2 mm to 8 mm in 2 mm steps (+3D/pl 2 mm, n = 6; +3D/pl 4 mm, n = 6; +3D/pl 6 mm, n = 8, or + 3D/pl 8 mm, n = 6). For the treatment lens with 2, 4, 6 and 8 mm central zones, objects at eccentricities beyond 11°, 16°, 19° and 23°, respectively, were imaged exclusively through the dual-power peripheral zones. Refractive status (retinoscopy), corneal power (keratometry) and axial dimensions (ultrasonography) were measured at two-week intervals. Comparison data were obtained from monkeys reared with binocular, single-vision +3D full-field lenses (+3D FF, n = 6) and 41 normal control monkeys reared with unrestricted vision. At the end of the rearing period, with the exception of the +3D/pl 8 mm group (median = +3.64 D), the ametropias for the other lens-reared groups (medians: FF = +4.39 D, 2 mm = +5.19 D, 4 mm = +5.59 D, 6 mm = +3.50 D) were significantly more hyperopic than that for the normal monkeys (+2.50 D). These hyperopic errors were associated with shallower vitreous chambers. The key finding was that the extent and consistency of these hyperopic ametropias varied with the eccentricity of the dual-focus zones. The results confirm that myopic defocus in the near periphery can slow axial growth, but that imposed defocus beyond about 20° from the fovea does not consistently alter central refractive development.

Studies in chickens suggest low intensity ambient lighting causes myopia. The purpose of this experiment was to examine the effects of low intensity ambient lighting (dim light) on normal refractive development in macaque monkeys. Seven infant rhesus monkeys were reared under dim light (room illumination level: ~55 lx) from 24 to ~310 days of age with otherwise unrestricted vision. Refractive error, corneal power, ocular axial dimensions, and choroidal thickness were measured in anesthetized animals at the onset of the experiment and periodically throughout the dim-light-rearing period, and were compared with those of normal-light-reared monkeys. We found that dim light did not produce myopia; instead, dim-light monkeys were hyperopic relative to normal-light monkeys (median refractive errors at ~155 days, OD: +3.13 D vs. +2.31 D; OS: +3.31D vs. +2.44 D; at ~310 days, OD: +2.75D vs. +1.78D, OS: +3.00D vs. +1.75D). In addition, dim-light rearing caused sustained thickening in the choroid, but it did not alter corneal power development, nor did it change the axial nature of the refractive errors. These results showed that, for rhesus monkeys and possibly other primates, low ambient lighting by itself is not necessarily myopiagenic, but might compromise the efficiency of emmetropization.

We investigated the potential causal relationships between anisometropia, amblyopia and strabismus, specifically to determine whether either amblyopia or strabismus interfered with emmetropization. We analyzed data from non-human primates that were relevant to the co-existence of anisometropia, amblyopia and strabismus in children. We relied on interocular comparisons of spatial vision and refractive development in animals reared with 1) monocular form deprivation; 2) anisometropia optically imposed by either contact lenses or spectacle lenses; 3) organic amblyopia produced by laser ablation of the fovea; and 4) strabismus that was either optically imposed with prisms or produced by either surgical or pharmacological manipulation of the extraocular muscles. Hyperopic anisometropia imposed early in life produced amblyopia in a dose-dependent manner. However, when potential methodological confounds were taken into account, there was no support for the hypothesis that the presence of amblyopia interferes with emmetropization or promotes hyperopia or that the degree of image degradation determines the direction of eye growth. To the contrary, there was strong evidence that amblyopic eyes were able to detect the presence of a refractive error and alter ocular growth to eliminate the ametropia. On the other hand, early onset strabismus, both optically and surgically imposed, disrupted the emmetropization process producing anisometropia. In surgical strabismus, the deviating eyes were typically more hyperopic than their fellow fixating eyes. The results show that early hyperopic anisometropia is a significant risk factor for amblyopia. Early esotropia can trigger the onset of both anisometropia and amblyopia. However, amblyopia, in isolation, does not pose a significant risk for the development of hyperopia or anisometropia.

We analyzed the contribution of individual ocular components to vision-induced ametropias in 210 rhesus monkeys. The primary contribution to refractive-error development came from vitreous chamber depth; a minor contribution from corneal power was also detected. However, there was no systematic relationship between refractive error and anterior chamber depth or between refractive error and any crystalline lens parameter. Our results are in good agreement with previous studies in humans, suggesting that the refractive errors commonly observed in humans are created by vision-dependent mechanisms that are similar to those operating in monkeys. This concordance emphasizes the applicability of rhesus monkeys in refractive-error studies.

Understanding the role of peripheral defocus on central refractive development is critical because refractive errors can vary significantly with eccentricity and peripheral refractions have been implicated in the genesis of central refractive errors in humans. Two rearing strategies were used to determine whether peripheral hyperopia alters central refractive development in rhesus monkeys. In intact eyes, lens-induced relative peripheral hyperopia produced central axial myopia. Moreover, eliminating the fovea by laser photoablation did not prevent compensating myopic changes in response to optically imposed hyperopia. These results show that peripheral refractive errors can have a substantial impact on central refractive development in primates.

PurposeDifferent subspecies of rhesus monkeys (Macaca mulatta) that are derived from different geographical locations, primarily Indian and China, are commonly employed in vision research. Substantial morphological and behavioral differences have been reported between Chinese- and Indian-derived subspecies. The purpose of this study was to compare refractive development in Chinese- and Indian-derived rhesus monkeys.MethodsThe subjects were 216 Indian-derived and 78 Chinese-derived normal infant rhesus monkeys. Cross-sectional data were obtained at 3 weeks of age for all subjects. In addition, longitudinal data were obtained from 10 Indian-derived (male=5, female=5) and 5 Chinese-derived monkeys (male=3, female=2) that were reared with unrestricted vision. Ocular and refractive development was assessed by retinoscopy, keratometry, video-based ophthalmophakometry, and A-scan ultrasonography.ResultsAlthough the course of emmetropization was very similar in these two groups of rhesus monkeys, there were consistent and significant inter-group differences in ocular dimensions and refractive error. Throughout the observation period, the Chinese-derived monkeys were on average about 0.4D less hyperopic than the Indian-derived monkeys and the Chinese-derived monkeys had longer overall axial lengths, deeper anterior and vitreous chamber depths, thicker crystalline lenses, flatter corneas and lower powered crystalline lenses.ConclusionsThe ocular differences observed in this study presumably reflect genetic differences between subspecies but could reflect the differences in the genetic pool between isolated colonies rather than true subspecies differences. Nonetheless, the substantial ocular differences that we observed emphasize that caution must be exercised when comparing and/or pooling data from rhesus monkeys obtained from different colonies. These inter-subspecies differences might be analogous to the ethnic differences in ocular parameters that have been observed in humans.

High-order monochromatic aberrations could potentially influence vision-dependent refractive development in a variety of ways. As a first step in understanding the effects of wave aberration on refractive development, we characterized the maturational changes that take place in the high-order aberrations of infant rhesus monkey eyes. Specifically, we compared the monochromatic wave aberrations of infant and adolescent animals and measured the longitudinal changes in the high-order aberrations of infant monkeys during the early period when emmetropization takes place. Our main findings were that (1) adolescent monkey eyes have excellent optical quality, exhibiting total RMS errors that were slightly better than those for adult human eyes that have the same numerical aperture and (2) shortly after birth, infant rhesus monkeys exhibited relatively larger magnitudes of high-order aberrations predominately spherical aberration, coma, and trefoil, which decreased rapidly to assume adolescent values by about 200 days of age. The results demonstrate that rhesus monkey eyes are a good model for studying the contribution of individual ocular components to the eye's overall aberration structure, the mechanisms responsible for the improvements in optical quality that occur during early ocular development, and the effects of high-order aberrations on ocular growth and emmetropization.

Purpose: Human infants exhibit a high prevalence of astigmatism. Although macaque monkeys are commonly used as animal models in experiments on early ocular growth and emmetropization, the prevalence of astigmatism in infant monkeys is unexplored. In this study we examine the prevalence and nature of astigmatism in infant monkeys.Methods: Refractive and corneal astigmatism were measured in 132, 2–5-week-old rhesus monkeys (Macaca mulatta) using cycloplegic retinoscopy and keratometry, respectively. Longitudinal measures of refractive development were obtained from 16 normal infants over the first 6 months of life.Results: Infant monkeys exhibited a low prevalence of astigmatism. Approximately 90% of the 2–5-week-old infants had 1.00 D (n=20), it was predominantly against-the-rule in nature (70.0%). The infant monkeys that were followed longitudinally rarely showed significant astigmatic errors at any time during the observation period. When these infant monkeys exhibited significant astigmatism, it was usually transient and not present on subsequent measurements.Conclusions: Unlike human infants, infant monkeys exhibit relatively little astigmatism. The low prevalence of astigmatism during early development suggests that astigmatism does not provide an essential cue for vision-dependent eye growth in infant primates.

The retinotopic map in the visual cortex of adult mammals can reorganize in response to a small injury in a restricted region of retina. Although the mechanisms underlying this neural plasticity in adults are not well understood, it is possible that rapid, adaptive alterations in the effectiveness of existing connections play a key role in the reorganization of cortical topography following peripheral deafferentation. In order to test this hypothesis, a small retinal lesion was made in one eye of adult cats and the visual cortex was mapped before and immediately after enucleating the non-lesioned eye. We found that substantial reorganization takes place within hours of enucleation.

The dependence of the emmetropization process on retinal ON-channel activity was examined in developing kittens by making regular intravitreal injections of D,L-2-amino-4-phosphonobutyric acid (APB). In comparison to sham-injected control eyes, the APB-treated eyes had shorter axial lengths and were more hyperopic. Since chronic atropinization did not alter the development of the APB-induced hyperopia, these anomalous refractive errors are not the result of altered accommodative function. The axial hyperopia observed in the APB-treated eyes indicates that the mechanisms responsible for normal axial elongation are dependent to some extent on ON-channel activity and that, even in the presence of a clear retinal image, OFF-channel activity, by itself, is not sufficient to regulate the normal emmetropization process.

The purpose of this study was to investigate the relationship between refractive errors and high-order aberrations in infant rhesus monkeys. Specifically, we compared the monochromatic wave aberrations measured with a Shack-Hartman wavefront sensor between normal monkeys and monkeys with vision-induced refractive errors. Shortly after birth, both normal monkeys and treated monkeys reared with optically induced defocus or form deprivation showed a decrease in the magnitude of high-order aberrations with age. However, the decrease in aberrations was typically smaller in the treated animals. Thus, at the end of the lens-rearing period, higher than normal amounts of aberrations were observed in treated eyes, both hyperopic and myopic eyes and treated eyes that developed astigmatism, but not spherical ametropias. The total RMS wavefront error increased with the degree of spherical refractive error, but was not correlated with the degree of astigmatism. Both myopic and hyperopic treated eyes showed elevated amounts of coma and trefoil and the degree of trefoil increased with the degree of spherical ametropia. Myopic eyes also exhibited a much higher prevalence of positive spherical aberration than normal or treated hyperopic eyes. Following the onset of unrestricted vision, the amount of high-order aberrations decreased in the treated monkeys that also recovered from the experimentally induced refractive errors. Our results demonstrate that high-order aberrations are influenced by visual experience in young primates and that the increase in high-order aberrations in our treated monkeys appears to be an optical byproduct of the vision-induced alterations in ocular growth that underlie changes in refractive error. The results from our study suggest that the higher amounts of wave aberrations observed in ametropic humans are likely to be a consequence, rather than a cause, of abnormal refractive development.

Purpose The purpose of this study was to characterize normal ocular development in infant monkeys and to establish both qualitative and quantitative relationships between human and monkey refractive development. Methods The subjects were 214 normal rhesus monkeys. Cross-sectional data were obtained from 204 monkeys at about 3 weeks of age and longitudinal data were obtained from 10 representative animals beginning at about 3 weeks of age for a period of up to 5 years. Ocular development was characterized via refractive status, corneal power, crystalline lens parameters, and the eye’s axial dimensions, which were determined by retinoscopy, keratometry, phakometry and A-scan ultrasonography, respectively. Results From birth to about 5 years of age, the growth curves for refractive error and most ocular components (excluding lens thickness and equivalent lens index) followed exponential trajectories and were highly coordinated between the two eyes. However, overall ocular growth was not a simple process of increasing the scale of each ocular component in a proportional manner. Instead the rates and relative amounts of change varied within and between ocular structures. Conclusion The configuration and contribution of the major ocular components in infant and adolescent monkey eyes are qualitatively and quantitatively very comparable to those in human eyes and their development proceeds in a similar manner in both species. As a consequence, in both species the adolescent eye is not simply a scaled version of the infant eye.

To shed light on the potential role of the phenomenon of form-deprivation myopia in normal refractive development, we investigated the degree of image degradation required to produce axial myopia in rhesus monkeys. Starting at about 3 weeks of age, diffuser spectacle lenses were employed to degrade the retinal image in one eye of 13 infant monkeys. The diffusers were worn continuously for periods ranging between 11 and 19 weeks. The effects of three different strengths of optical diffusers, which produced reductions in image contrast that ranged from about 0.5 to nearly 3 log units, were assessed by retinoscopy and A-scan ultrasonography. Control data were obtained from ten normal infants and three infants reared with clear, zero-powered lenses over both eyes. Eleven of the 13 treated infants developed form-deprivation myopia. Qualitatively similar results were obtained for the three diffuser groups, however, the degree of axial myopia varied directly with the degree of image degradation. Thus, form-deprivation myopia in monkeys is a graded phenomenon and can be triggered by a modest degree of chronic image degradation.

Early in life, the two eyes of infant primates normally grow in a coordinated manner toward the ideal refractive state. We investigated the extent to which lens-induced changes in the effective focus of the eye affected refractive development in infant rhesus monkeys. The main finding was that spectacle lenses could predictably alter the growth of one or both eyes resulting in appropriate compensating refractive changes in both the hyperopic and myopic directions. Although the effective operating range of the emmetropization process in young monkeys is somewhat limited, the results demonstrate that emmetropization in this higher primate, as in a number of other species, is an active process that is regulated by optical defocus associated with the eye’s effective refractive state.

Investigations on macaque monkeys have provided much of our knowledge of the neural mechanisms of binocular vision, but there is little psychophysical data on the accuracy of vergence responses or the precision of stereoscopic depth perception in these primates. We have conducted comparative behavioral studies of binocular disparity processing in rhesus monkeys and humans via measurements of prism-induced fixation disparities (disparity vergence) and relative depth discrimination for spatially localized stimuli (local stereopsis). The results of these studies demonstrated a remarkable similarity in both the oculomotor and the sensory aspects of binocular vision in the two species when the stimulus dimensions were specified in visual angels, which were independent of interocular separation. The disparity vergence functions for the two species revealed fusion responses over the same range of prism-induced vergence and comparable vergence errors for stimuli near their fusional limits. Disparity vergence responses were independent of the spatial frequency of the binocular fusion stimulus. Stereothresholds as a function of the spatial frequency of the difference-of-Gaussian stimuli were of the same form, with equivalent stereoacuities, in monkey and human observers. The presence of substantial vergence errors had only a small effect on the precision of stereoscopic depth perception. We conclude that, after compensation for the differences in the lateral separation of their eyes, the operating characteristics of disparity vergence and stereoscopic vision are virtually identical in rhesus monkeys and humans and, consequently, the performance limits for these visual functions must be determined by anatomical and/or neural constraints that are similar in both species.

In each of eight rhesus monkeys, one eye was defocused with a -9 D contact lens beginning before 1 month of age for periods of 2-3 months. At the end of the rearing period, interocular comparisons showed that one subject had developed a relative axial myopia (3.0 D), however, five monkeys had developed a relative axial hyperopia (2.0-3.5 D). After discontinuing the contact-lens rearing procedure, the induced refractive errors diminished over time in all subjects. These results indicate that the defocus threshold for form-deprivation myopia is relatively high and that substantial levels of optical defocus which do not exceed this threshold typically produce axial hyperopia. The recovery data suggests that monkeys have an emmetropization mechanism which is sensitive to optical defocus, but the failure of this mechanism to compensate for the refractive errors simulated during the lens-rearing procedures suggests that this mechanism has a limited operating range.

A number of electrophysiological studies have shown sustained and transient neurons in the monkey visual system. These findings are consistent with the large number of psychophysical experiments in which the data are best interpreted on the basis of sustained and transient channels in the human visual system. In the present study, three experimental procedures which have provided strong evidence for sustained and transient channels for human observers were replicated using 4 rhesus monkeys as subjects. All three procedures were based on detection of grating patterns generated on the CRT of an oscilloscope. Data were collected to obtain (1) reaction time distributions for near threshold contrast levels as a function of the spatial frequency of the gratings, (2) contrast sensitivity as a function of viewing duration for several spatial frequencies and (3) mean reaction time as a function of contrast for suprathreshold gratings. The reaction time histograms for near threshold stimuli showed a bimodal distribution of reaction times for low spatial frequencies and a unimodal distribution for higher spatial frequencies. The contrast sensitivity versus viewing duration curves showed that the slope of the function above a critical duration was nearly zero for low spatial frequencies and had a slope of approx 0.3 for higher spatial frequencies. The suprathreshold reaction time data showed a biphasic function for midrange spatial frequencies, but a monophasic function for high and low spatial frequencies. The data from all 3 experiments were consistent with similar data reported for human subjects and, therefore, to the extent that human data reflect the existence of sustained and transient channels, so do the monkey data.

Increment contrast thresholds were determined behaviourally as a function of background contrast for sinusoidal gratings with spatial frequencies between 0.5 and 8.0 c/deg. As has been previously reported for humans, the contrast discrimination functions were characterized by a facilitation effect for low background contrasts and a masking effect for high background contrasts. The shapes of the functions varied with spatial frequency, but for all spatial frequencies, portions of the functions were adequately described by a power law. The shapes of the reaction time distributions obtained for near threshold stimuli suggested that at least two mechanisms with different spatio-temporal sensitivities were involved in detecting the stimulus and that the exact shape of the contrast discrimination function was dependent on which mechanism dominated detection.

Spatial modulation sensitivity functions have been investigated by behavioral methods in two monkeys reared with normal visual experience and 12 monkeys reared with abnormal, early visual experience. Experimental treatments were initiated when the animals were approximately one month of age. Two monkeys were each treated with one of the following procedures: (1) long-term monocular lid suture, (2) short-term monocular lid suture, (3) surgically induced esotropia, (4) surgically induced exotropia, (5) optical dissociation of binocular vision with ophthalmic prisms, or (6) chronic monocular cycloplegia. The results of the studies showed a severe loss of contrast sensitivity of the treated eyes compared to the control eyes for monkeys reared with monocular lid suture or surgically induced esotropia. Surgically induced exotropia resulted in a moderate reduction in sensitivity of the deviated eye while optical dissociation resulted in a mild reduction in sensitivity of one eye compared to the other. One of the two monkeys reared for seven months with chronic monocular cycloplegia had a relative reduction in contrast sensitivity of the treated eye, but the other monkey had equal sensitivities in the two eyes. However, binocular summation experiments showed that even though the relative difference between the monocular sensitivities was small or absent for the monkeys reared with optical dissociation or chronic monocular cycloplegia, none of them demonstrated binocular vision in these experiments.

Lid closure initiated early in life produces axial myopia in a variety of species. However, it is currently not known what aspects of the anomalous visual experience associated with lid closure disrupt the emmetropization process and cause abnormal ocular axial elongation. This study was designed to determine if a degradation in the quality of the spatial characteristics of the retinal image was sufficient to produce an experimental myopia. Optical rearing procedures were employed to defocus one eye of developing kittens, and retinoscopic and ultrasonic procedures were used to evaluate the effects of chronic optical defocus on the kitten's refractive status. Different defocusing lens designs and rearing protocols were included to evaluate variables that may have confounded previous investigations. The major finding is that early chronic optical defocus results in axial myopia. The prevalence and magnitude of the induced refractive errors were dependent on the magnitude of optical defocus, but they were not affected by the sign or form of the defocusing lens. The results demonstrated that the potential for a clear retinal image is important for regulating normal ocular growth and maintaining a near emmetropic refractive status.

The extent of voluntary accommodation was investigated behaviorally in two young rhesus monkeys and an adult human using a modified minus-lens technique. Specifically, contrast sensitivity for a high spatial frequency grating was determined as a function of spectacle lens power. Accommodative amplitudes derived from contrast sensitivity vs lens power functions indicate that young monkeys have at least 17 to 18 D of voluntary accommodation and that the accommodative amplitudes of monkeys are larger than those of equivalent-aged humans.

To determine whether developing primate eyes are capable of growing in a manner that eliminates astigmatism, we reared infant monkeys with cylindrical spectacle lenses in front of one or both eyes that optically simulated with-the-rule, against-the-rule, or oblique astigmatism (+1.50−3.00×90, ×180, ×45 or ×135). Refractive development was assessed by retinoscopy, keratometry and A-scan ultrasonography. In contrast to control monkeys, the cylinder-lens-reared monkeys developed significant amounts of astigmatism. The astigmatism was corneal in nature, bilaterally mirror symmetric and oblique in axis, and reversible. The ocular astigmatism appeared to be due to a reduction in the rate of corneal flattening along the steeper meridian while the other principal meridian appeared to flatten at a more normal rate. However, regardless of the orientation of the optically imposed astigmatism, the axis of the ocular astigmatism was not appropriate to compensate for the astigmatic error imposed by the treatment lenses. Our results indicate that visual experience can alter corneal shape, but there was no evidence that primates have an active, visually regulated “sphericalization” mechanism.

The surgical treatment for strabismus in infants generally results in microtropia or subnormal binocular vision. Although the clinical characteristics of these conditions are well established, there are important questions about the mechanisms of binocular vision in these patients that can best be investigated in an appropriate animal model. In the present psychophysical investigations, spatial frequency response functions for disparity-induced fusional vergence and for local stereopsis were studied in macaque monkeys, who demonstrated many of the major visual characteristics of patients whose eyes were surgically aligned during infancy. In six rhesus monkeys, unilateral esotropia was surgically induced at various ages (30–184 days of age). However, over the next 12 months, all of the monkeys recovered normal eye alignment. Behavioral measurements at 4–6 years of age showed that the monkeys' prism-induced fusional vergence responses were indistinguishable from those of control monkeys or humans with normal binocular vision. Investigations of stereo-depth discrimination demonstrated that each of the experimental monkeys also had stereoscopic vision, but their stereoacuities varied from being essentially normal to severely stereo-deficient. The degree of stereo-deficiency was not related to the age at which surgical esotropia was induced, or to the presence or absence of amblyopia, and was not dependent on the spatial frequency of the test stimulus. Altogether, these experiments demonstrate that a temporary, early esotropia can affect the binocular disparity responses of motor and sensory components of binocular vision differently, probably because of different sensitive periods of development for the two components. Copyright © 1997 Elsevier Science Ltd

With normal binocular vision, maximal stereoacuity requires an extended viewing duration, but the relationship between the critical viewing duration for stereopsis and other variables affecting stereoacuity is unknown. The purposes of the study were to investigate the properties of normal temporal integration for stereoscopic vision with respect to the effects of contrast and spatial frequency of the stimuli and to determine whether the temporal summation of disparity is affected in deficient stereopsis caused by abnormal binocular vision during infancy. Psychophysical methods were used to measure stereothresholds in human and monkey subjects with either normal binocular vision or abnormal binocular vision. The results showed that the critical viewing duration for stereoscopic depth discrimination was independent of variations in basic stimulus parameters and/or the subject’s stereoacuity. A critical duration of approximately 100 ms was found for both local (narrowband Gabor and broadband line targets) and global (dynamic random dots) stimuli. Although stereothresholds increased with decreasing stimulus contrast, the properties of temporal integration did not. Stereothresholds were substantially elevated for monkeys and humans with abnormal binocular vision, but the critical durations for these subjects were not significantly different from those of subjects with normal binocular vision. Overall, the results demonstrate that the general properties of temporal integration for stereopsis are similar to other detection and discrimination tasks that do not require binocular processing. In addition, increased integration time does not account for the elevated stereothresholds of subjects with abnormal binocular vision.

To determine if monkeys exhibit clinical suppression in response to early abnormal binocular vision, we compared dichoptic to monocular luminance increment thresholds in monkeys reared with alternating monocular defocus or optically induced strabismus. In the absence of amblyopia, clinical suppression was associated with strabismus and with as little as 1.50 diopters of anisometropia. The severity of suppression was roughly correlated with the magnitude of anisometropia. The demonstration of clinical suppression in monkeys provides a model for future investigations of factors that may influence the development of suppression, but which are not possible to accurately document or manipulate in human subjects.

Contrast sensitivity and increment-threshold functions were studied for three rhesus monkeys with stimulus deprivation amblyopia. The monkeys' right eyelids were sutured closed before the age of 1 month for periods of two weeks, 19 months and 23 months. Contrast sensitivity measurements for all three monkeys showed greatly reduced visual function in the deprived eye with a high spatial frequency cut-off 6 octaves lower in the deprived than the nondeprived eyes. The increment-threshold data collected for the two long-term lid-sutured monkeys showed both photopic and scotopic abnormalities in the deprived eyes. For example, with complete dark adaptation although the spectral sensitivity data for both the deprived and nondeprived eyes were well fit by the scotopic luminosity function, the sensitivity for the deprived eye was approximately 4 log units lower than the nondeprived eye. In addition, the spectral sensitivity data for the deprived eyes showed scotopic luminosity functions for achromatic adapting field luminances of 188, 750 and 3000 td whereas the nondeprived eye showed normal photopic function for all light adapted conditions. Even when the spectral sensitivity measurements were made in the presence of intense blue backgrounds, the data obtained for the deprived eyes were best described as showing scotopic function over the short wavelengths and photopic function only at the longer wavelengths. The increment-threshold functions for achromatic stimuli showed normal rod-cone interactions in the nondeprived eyes, but the functions were monotonic for the deprived eyes over a 9 log unit range of background luminances. Therefore, the results of these experiments show that stimulus deprivation causes profound defects for visual resolution, rod saturation and the rate of change of sensitivity with light adaptation.