Biomedical subjects

Earl L Smith

Publications and source records attributed to Earl L Smith.

At least 19 recordsLinked to original sources

PubMed2006

Monochromatic ocular wave aberrations in young monkeys.

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.

Accommodation, Ocular↗

PubMed2006

Brief daily periods of unrestricted vision can prevent form-deprivation amblyopia.

PURPOSE: To characterize how the mechanisms that produce unilateral form-deprivation amblyopia integrate the effects of normal and abnormal vision over time, the effects of brief daily periods of unrestricted vision on the spatial vision losses produced by monocular form deprivation were investigated in infant monkeys. METHODS: Beginning at 3 weeks of age, unilateral form deprivation was initiated in 18 infant monkeys by securing a diffuser spectacle lens in front of one eye and a clear plano lens in front of the fellow eye. During the treatment period (18 weeks), three infants wore the diffusers continuously. For the other experimental infants, the diffusers were removed daily and replaced with clear, zero-powered lenses for 1 (n=5), 2 (n=6), or 4 (n=4) hours. Four infants reared with binocular zero-powered lenses and four normally reared monkeys provided control data. RESULTS: The degree of amblyopia varied significantly with the daily duration of unrestricted vision. Continuous form deprivation caused severe amblyopia. However, 1 hour of unrestricted vision reduced the degree of amblyopia by 65%, 2 hours reduced the deficits by 90%, and 4 hours preserved near-normal spatial contrast sensitivity. CONCLUSIONS: The severely amblyogenic effects of form deprivation in infant primates are substantially reduced by relatively short daily periods of unrestricted vision. The manner in which the mechanisms responsible for amblyopia integrate the effects of normal and abnormal vision over time promotes normal visual development and has important implications for the management of human infants with conditions that potentially cause amblyopia.

Amblyopia↗

PubMed2005

Rapid plasticity of binocular connections in developing monkey visual cortex (V1).

The basic sets of cortical connections are present at birth in the primate visual system. The maintenance and refinement of these innate connections are highly dependent on normal visual experience, and prolonged exposure to binocularly uncorrelated signals early in life severely disrupts the normal development of binocular functions. However, very little is known about how rapidly these changes in the functional organization of primate visual cortex emerge or what are the sequence and the nature of the abnormal neural events that occur immediately after experiencing binocular decorrelation. In this study, we investigated how brief periods of ocular misalignment (strabismus) at the height of the critical period alter the cortical circuits that support binocular vision. After only 3 days of optically imposed strabismus, there was a striking increase in the prevalence of V1 neurons that exhibited binocular suppression, i.e., binocular responses were weaker than monocular responses. However, the sensitivity of these neurons to interocular spatial phase disparity was not significantly altered. These contrasting results suggest that the first significant change in V1 caused by early binocular decorrelation is binocular suppression, and that this suppression originates at a site(s) beyond where binocular signals are initially combined.

Animals↗

PubMed2005

Delayed maturation of receptive field center/surround mechanisms in V2.

Neurons in the adult visual cortex are capable of integrating signals over a large area that surrounds their classic receptive field (RF), and this ability of cortical neurons is thought to be intimately involved in perceptual binding. It is not known, however, at what age these long-range signal interactions emerge. Here, we report that qualitatively adult-like center/surround interactions are already present in the primary visual cortex as early as postnatal day 14 in macaque monkeys. However, the RF surrounds of visual area 2 (V2) neurons were largely absent until 4 weeks of age and, as late as 8 weeks of age, center/surround signal interactions in V2 neurons were immature. Our results suggest that the cortical circuits underlying the RF center/surround of individual neurons mature considerably later in V2 than in the primary visual cortex and give critical evidence for the hypothesis that the functional maturation of the primate visual brain proceeds in a hierarchical manner.

Age Factors↗

PubMed2005

Astigmatism in monkeys with experimentally induced myopia or hyperopia.

PURPOSE: Astigmatism is the most common ametropia found in humans and is often associated with large spherical ametropias. However, little is known about the etiology of astigmatism or the reason(s) for the association between spherical and astigmatic refractive errors. This study examines the frequency and characteristics of astigmatism in infant monkeys that developed axial ametropias as a result of altered early visual experience. METHODS: Data were obtained from 112 rhesus monkeys that experienced a variety of lens-rearing regimens that were intended to alter the normal course of emmetropization. These visual manipulations included form deprivation (n = 13); optically imposed defocus (n = 48); and continuous ambient lighting with (n = 6) or without optically imposed defocus (n = 6). In addition, data from 19 control monkeys and 39 infants reared with an optically imposed astigmatism were used for comparison purposes. The lens-rearing period started at approximately 3 weeks of age and ended by 4 to 5 months of age. Refractive development for all monkeys was assessed periodically throughout the treatment and subsequent recovery periods by retinoscopy, keratometry, and A-scan ultrasonography. RESULTS: In contrast to control monkeys, the monkeys that had experimentally induced axial ametropias frequently developed significant amounts of astigmatism (mean refractive astigmatism = 0.37 +/- 0.33 D [control] vs. 1.24 +/- 0.81 D [treated]; two-sample t-test, p < 0.0001), especially when their eyes exhibited relative hyperopic shifts in refractive error. The astigmatism was corneal in origin (Pearson's r; p < 0.001 for total astigmatism and the JO and J45 components), and the axes of the astigmatism were typically oblique and bilaterally mirror symmetric. Interestingly, the astigmatism was not permanent; the majority of the monkeys exhibited substantial reductions in the amount of astigmatism at or near the end of the lens-rearing procedures. CONCLUSIONS: In infant monkeys, visual conditions that alter axial growth can also alter corneal shape. Similarities between the astigmatic errors in our monkeys and some astigmatic errors in humans suggest that vision-dependent changes in eye growth may contribute to astigmatism in humans.

Animals↗

PubMed2005

Scaling the structure--function relationship for clinical perimetry.

PURPOSE: The full ranges of glaucomatous visual field defects and retinal ganglion cell losses extend over several orders of magnitude and therefore an interpretation of the structure-function relationship for clinical perimetry requires scaling of both variables. However, the most appropriate scale has not been determined. The present study was undertaken to compare linear and logarithmic transformations, which have been proposed for correlating the perimetric defects and neural losses of glaucoma. METHODS: Perimetry, by behavioural testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma. Ganglion cell densities were measured in histologic sections of retina that corresponded to specific perimetry test locations for the treated and control eyes. The linear (percentage) and logarithmic (decibel) relationships for sensitivity loss as a function of ganglion cell loss were analysed. RESULTS: With decibel scaling, visual sensitivity losses and ganglion cell densities were linearly correlated with high coefficients of determination (r(2)), although the parameters of the functions varied with eccentricity. The structure-function relationships expressed as linear percentage-loss functions were less systematic in two respects. Firstly, the relationship exhibited considerable scatter in the data for small losses in visual sensitivity and, secondly, visual sensitivity losses became saturated with larger losses in ganglion cell density. The parameters of the percentage-loss functions also varied with eccentricity, but the variation was less than for the decibel-loss functions. CONCLUSIONS: Linear scaling of perimetric defects and ganglion cell losses might potentially improve the structure-function relationship for visual defects associated with small amounts of cell loss, but the usefulness of the relationship is limited because of the high variability in that range. With log--log co-ordinates, the structure--function relationship for clinical perimetry is relatively more accurate and precise for cell losses greater than about 3 dB. The comparatively greater accuracy and precision of decibel loss functions are a likely consequence of the logarithmic scale of stimulus intensities for perimetry measurements and because the relationship between visual sensitivity and the number of neural detectors is a form of probability summation.

Animals↗

PubMed2005

Peripheral vision can influence eye growth and refractive development in infant monkeys.

PURPOSE: Given the prominence of central vision in humans, it has been assumed that visual signals from the fovea dominate emmetropization. The purpose of this study was to examine the impact of peripheral vision on emmetropization. METHODS: Bilateral, peripheral form deprivation was produced in 12 infant monkeys by rearing them with diffusers that had either 4- or 8-mm apertures centered on the pupils of each eye, to allow 24 degrees or 37 degrees of unrestricted central vision, respectively. At the end of the lens-rearing period, an argon laser was used to ablate the fovea in one eye of each of seven monkeys. Subsequently, all the animals were allowed unrestricted vision. Refractive error and axial dimensions were measured along the pupillary axis by retinoscopy and A-scan ultrasonography, respectively. Control data were obtained from 21 normal monkeys and 3 infants reared with binocular plano lenses. RESULTS: Nine of the 12 treated monkeys had refractive errors that fell outside the 10th- and 90th-percentile limits for the age-matched control subjects, and the average refractive error for the treated animals was more variable and significantly less hyperopic/more myopic (+0.03 +/- 2.39 D vs. +2.39 +/- 0.92 D). The refractive changes were symmetric in the two eyes of a given animal and axial in nature. After lens removal, all the treated monkeys recovered from the induced refractive errors. No interocular differences in the recovery process were observed in the animals with monocular foveal lesions. CONCLUSIONS: On the one hand, the peripheral retina can contribute to emmetropizing responses and to ametropias produced by an abnormal visual experience. On the other hand, unrestricted central vision is not sufficient to ensure normal refractive development, and the fovea is not essential for emmetropizing responses.

Animals↗

PubMed2005

Directional bias of neurons in V1 and V2 of strabismic monkeys: temporal-to-nasal asymmetry?

PURPOSE: Strabismus that develops shortly after birth is known to cause temporal-to-nasal eye movement asymmetries under monocular viewing. The neural mechanisms underlying this deficit are not well understood. In the current study, the hypothesis that this eye movement anomaly reflects a similar asymmetry in the directional response properties of neurons in the early stages of cortical processing was examined. METHODS: Strabismus was simulated with optical methods in infant monkeys between 4 and 14 weeks of age. When the monkeys were mature, microelectrode recording experiments were conducted in the primary visual cortex (V1) and visual area 2 (V2). After the spatial frequency of sine wave-grating stimuli for each neuron was optimized, each neuron's responsiveness to 24 directions of stimulus movement was measured. The preferred direction and the strength of directional bias were determined by a vector summation method: RESULTS: There was not an overabundance of neurons in V1 or V2 of strabismic monkeys preferring the temporal-to-nasal direction of stimulus movement. However, the average directional bias was significantly reduced in these strabismic monkeys. Interocular suppression was highly prevalent, and this suppression was stronger and more common in neurons dominated by the ipsilateral eye. CONCLUSIONS: The results suggest that the eye movement asymmetries in strabismic subjects do not result from similar asymmetries in the directional properties of V1 or V2 neurons, but rather reflect impoverished cortical signals to the brain stem nuclei that control eye movements.

Animals↗

PubMed2004

Glutathione content is altered in Müller cells of monkey eyes with experimental glaucoma.

Extracellular levels of glutamate are thought to be increased in glaucoma and thus contribute to retinal damage. An increase in glutamate concentration or duration in the extracellular retinal space is expected to impact glutathione content in Müller cells since glutamate is the rate-limiting constituent in glutathione synthesis. We have investigated whether glutathione content is changed in retinal Müller cells of monkeys with experimental glaucoma using immunocytochemistry and image analysis. Müller cells in glaucomatous retinas showed significantly greater immunoreactivity (27-57%) for glutathione than those in fellow control retinas, increasing with the duration of elevated intraocular pressure (IOP). This pattern of labeling was prominent in all four monkeys studied. The presence of more glutathione in Müller cells of glaucomatous retinas is consistent with an increase in extracellular glutamate and an increase in transport and metabolism of glutamate.

Animals↗

PubMed2004

Effects of optically imposed astigmatism on emmetropization in infant monkeys.

PURPOSE: Although astigmatism is prevalent during early infancy, the influence of astigmatism on early refractive development is unclear. This study was undertaken to determine the effects of astigmatism on emmetropization in monkeys. METHODS: Infant rhesus monkeys (n = 39) were exposed to optically simulated astigmatism in one or both eyes from approximately 1 to 4 months of age. With-the-rule, against-the-rule, and oblique astigmatisms were optically simulated by appropriately orienting the principal meridians of the spherocylindrical treatment lenses (+1.50 -3.00 D x 90 degrees, 180 degrees, 45 degrees, or 135 degrees; i.e., +1.50 and -1.50 D powers in the two principal meridians). Refractive development was assessed every 2 to 3 weeks by cycloplegic retinoscopy, keratometry and corneal videotopography, and A-scan ultrasonography. Data from 19 control monkeys, including 3 animals that were reared with binocular plano lenses, were used for comparison purposes. RESULTS: Most of the cylinder-lens-reared monkeys, regardless of the orientation of the imposed astigmatism, showed clear signs of either hyperopic or myopic growth compared with control monkeys. The distributions of refractive error and vitreous chamber depth both showed bimodal patterns that differed from normal by amounts equivalent to the optical powers of the principal meridians of the treatment lenses. More frequently, refractive development was biased toward the eye's least-hyperopic focal plane. The refractive changes were mainly axial. After lens removal, the lens-reared monkeys recovered and as a group exhibited refractive errors and axial dimensions similar to those in control monkeys. CONCLUSIONS: In the presence of significant amounts of astigmatism, emmetropization is directed toward one of the two focal planes associated with the astigmatic principal meridians and not the circle of least confusion. These results suggest that the mechanisms responsible for emmetropization are insensitive to stimulus orientation and the global form of the retinal image. It appears that emmetropization seeks out the image plane that contains the maximum effective contrast integrated across spatial frequency and stimulus orientation.

Animals↗

PubMed2004

Image defocus modulates activity of bipolar and amacrine cells in macaque retina.

PURPOSE: To demonstrate regulation of ocular growth and refractive development by image quality and processing in the retina in higher primates. Focus-sensitive retinal neurons were labeled with immunocytochemical markers after briefly altering image quality in infant monkeys. METHODS: Six rhesus monkeys (Macaca mulatta) 20- to 30-days-old were fitted with goggles after 6 hours in the light. Three wore a +3 D lens and three a diffuser on the treated eye; contralateral control eyes wore plano lenses matched in transmission to the goggles on treated eyes. After 30, 60, or 240 minutes exposure, the animals were killed, the eyes opened and fixed in 4% formaldehyde, and cryosections labeled with antibodies to inducible activity markers (transcription factors Egr-1 and Fra-2) and type-specific amacrine cell markers. Labeled cells were identified and counted in a fluorescence microscope, and the spatial density of activity-labeled nuclei and the frequency of activity-labeling of specific amacrine cells were determined, without knowing treated eye or duration. RESULTS: Focus-sensitive immunoreactivity was demonstrated for Egr-1 and Fra-2 in a GAD65-immunoreactive (IR) subpopulation of GABAergic amacrine cells, and for Egr-1 alone in PKC alpha-, 115A10-, and CD15-IR ON-bipolar cells. Activity of ON-bipolar and GABAergic amacrine cells, as indicated by Egr-1 induction, was stimulated more by in-focus or myopically-defocused images than by hyperopically-defocused or diffusely blurred images, regardless of exposure duration. CONCLUSIONS: This was the first evidence of focus-dependent activation of bipolar as well as amacrine cells in a primate retina. Focus-sensitive neurons are candidates for roles in vision-dependent regulation of eye growth.

Amacrine Cells↗

PubMed2004

Recovery from form-deprivation myopia in rhesus monkeys.

PURPOSE: Although many aspects of vision-dependent eye growth are qualitatively similar in many species, the failure to observe recovery from form-deprivation myopia (FDM) in higher primates represents a significant potential departure. The purpose of this investigation was to re-examine the ability of rhesus monkeys (Macaca mulatta) to recover from FDM. METHODS: Monocular form deprivation was produced either with diffuser spectacle lenses (n = 30) or by surgical eyelid closure (n = 14). The diffuser-rearing strategies were initiated at 24 +/- 3 days of age and continued for an average of 115 +/- 20 days. Surgical eyelid closure was initiated between 33 and 761 days of age and maintained for14 to 689 days. After the period of form deprivation, the animals were allowed unrestricted vision. The ability of the animals to recover from treatment-induced refractive errors was assessed periodically by retinoscopy, keratometry, and A-scan ultrasonography. Control data were obtained from 35 normal monkeys. RESULTS: At the onset of unrestricted vision, the deprived eyes of 18 of the diffuser-reared monkeys and 12 of the lid-sutured monkeys were at least 1.0 D less hyperopic or more myopic than their fellow eyes. The mean (diffuser = -4.06 D, lid-suture = -4.50 D) and range (diffuser = -1.0 to -10.19 D, lid-suture = -1.0 to -10.25 D) of myopic anisometropia were comparable in both treatment groups. All 18 of these diffuser-reared monkeys demonstrated recovery, with 12 animals exhibiting complete recovery. The rate of recovery, which was mediated primarily by alterations in vitreous chamber growth rate, declined with age. None of the lid-sutured monkeys exhibited clear evidence of recovery. Instead, 8 of the 12 lid-sutured monkeys exhibited progression of myopia. CONCLUSIONS: Like many other species, young monkeys are capable of recovering from FDM. However, the potential for recovery appears to depend on when unrestricted vision is restored, the severity of the deprivation-induced axial elongation, and possibly the method used to produce FDM.

Animals↗

PubMed2004

Compensation for experimentally induced hyperopic anisometropia in adolescent monkeys.

PURPOSE: Early in life, the optical demand associated with the eye's effective refractive state regulates emmetropization in many species, including primates. However, the potential role of optical demand and/or defocus in the genesis of common refractive errors, like myopia, that normally develop much later in life is not known. The purpose of this study was to determine whether chronic optical defocus alters refractive development in monkeys at ages corresponding to when myopia typically develops in children. METHODS: A hyperopic anisometropia was produced in seven adolescent rhesus monkeys by photorefractive keratectomy (PRK) with an excimer laser. Standard treatment algorithms for correcting myopia in humans were used to selectively flatten the central cornea of one eye thereby producing relative hyperopic refractive errors in the treated eyes. The laser ablation zones were 5.0 mm in diameter and centered on the monkeys' pupils. The laser procedures were performed when the monkeys were 2 to 2.5 years old, which corresponded to onset ages between approximately 8 and 10 human years. The ocular effects of the induced anisometropia were assessed by corneal topography, retinoscopy, and A-scan ultrasonography. RESULTS: By approximately 30 days after PRK, the experimentally induced refractive errors had stabilized and the treated eyes were between +0.75 and +2.25 D more hyperopic than their fellow eyes. Subsequently, over the next 300 to 400 days, six of the seven monkeys showed systematic reductions in the degree of anisometropia. Although some regression in corneal power occurred, the compensating refractive changes were primarily due to relative interocular differences in vitreous chamber growth. CONCLUSIONS: Vision-dependent mechanisms that are sensitive to refractive error are still active in adolescent primates and probably play a role in maintaining stable refractive errors in the two eyes. Consequently, conditions that result in consistent hyperopic defocus could potentially contribute to the development of juvenile onset myopia in children.

Animals↗

PubMed2004

Neural losses correlated with visual losses in clinical perimetry.

PURPOSE: The validity of clinical perimetry for evaluation of the pathology of glaucoma is based on correlated losses in retinal ganglion cells and visual sensitivity, but procedures to quantify neural losses from visual field defects have not been developed. The purpose of the present study was to investigate the neural and sensitivity losses from experimental glaucoma to establish the framework for a quantitative model for the structure-function relationships of standard clinical perimetry. METHODS: Perimetry, by behavioral testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma. Ganglion cell densities were obtained from sections of retina that corresponded to 16 perimetry test locations. Perimetry sensitivity as a function of ganglion cell density at corresponding retina/visual field locations was analyzed. RESULTS: The structure-function relationships were linear on log-log coordinates, with parameters that varied systematically with eccentricity. The slope value varied from 1.25 dB/dB at 4.2 degrees from fixation to a value of 2.32 dB/dB at 24 degrees from fixation, whereas the intercept value varied from -25.2 dB to -55.7 dB over the same range of eccentricities. The structure-function relationships produced a model to predict the ganglion cell density underlying a given level of visual sensitivity and location in the visual field. The model, with no free parameters, produced an accurate and relatively precise quantification of retinal ganglion cell losses caused by experimental glaucoma in monkeys. However, because the early detection of glaucoma is limited by intersubject variability, ganglion cell losses of 40% to 50% were necessary before visual sensitivity losses exceeded the normal 95% confidence limits. CONCLUSIONS: With retinal eccentricity as a factor, the neural losses from glaucoma are predictable from visual sensitivity measurements by clinical perimetry. The relationships derived from experimental glaucoma in monkeys also accurately predict the rate of age-related losses of retinal ganglion cells in humans, based on the normative perimetry data for age-related reductions in visual sensitivity. The success of the model in this study suggested that it is potentially applicable to the clinical interpretation of the state of glaucomatous optic neuropathy.

Animals↗

PubMed2003

Temporal integration for stereoscopic vision.

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.

Animals↗

PubMed2003

Astigmatism in infant monkeys reared with cylindrical lenses.

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 (+1.50-3.00x90, x180, x45 or x135). 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.

Adaptation, Physiological↗

PubMed2003

Continuous ambient lighting and lens compensation in infant monkeys.

PURPOSE: Protracted daily lighting cycles do not promote abnormal ocular enlargement in infant monkeys as they do in a variety of avian species. However, observations in humans suggest that ambient lighting at night may reduce the efficiency of the emmetropization process in primates. To test this idea, we investigated the ability of infant monkeys reared with continuous light to compensate for optically imposed changes in refractive error. METHODS: Beginning at about 3 weeks of age, a hyperopic or myopic anisometropia was imposed on 12 infant rhesus monkeys by securing either a -3 D or +3 D lenses in front of one eye and a zero-powered lens in front of the fellow eye. Six of these monkeys were reared with the normal vivarium lights on continuously, whereas the other six lens-reared monkeys were maintained on a 12-h-light/12-h-dark lighting cycle. The ocular effects of the lens-rearing procedures were assessed periodically during the treatment period by cycloplegic retinoscopy, keratometry, and A-scan ultrasonography. RESULTS: Five of six animals in each of the lighting groups demonstrated clear evidence for compensating anisometropic growth. In both lighting groups, eyes that experienced optically imposed hyperopic defocus (-3 D lenses) exhibited faster axial growth rates and became more myopic than their fellow eyes. In contrast, eyes treated with +3 D lenses showed relatively slower axial growth rates and developed more hyperopic refractive errors. The average amount of compensating anisometropia (continuous light, 1.6 +/- 0.5 D vs. control, 2.3 +/- 0.5 D), the structural basis for the refractive errors, and the ability to recover from the induced refractive errors were also not altered by continuous light exposure. CONCLUSION: Ambient lighting at night does not appear to overtly compromise the functional integrity of the vision-dependent mechanisms that regulate emmetropization in higher primates.

Animals↗

PubMed2003

Binocular deficits associated with early alternating monocular defocus. II. Neurophysiological observations.

Experiencing binocularly conflicting signals early in life dramatically alters the binocular responses of cortical neurons. Because visual cortex is highly plastic during a critical period of development, cortical deficits resulting from early abnormal visual experience often mirror the nature of interocular decorrelation of neural signals from the two eyes. In the preceding paper, we demonstrated that monkeys that experienced early alternating monocular defocus (-1.5, -3.0, or -6.0 D) show deficits in stereopsis that generally reflected the magnitude of imposed monocular defocus. Because these results indicated that alternating monocular defocus affected the higher spatial frequency components of visual scenes more severely, we employed microelectrode recording methods to investigate whether V1 neurons in these lens-reared monkeys exhibited spatial-frequency-dependent alterations in their binocular response properties. We found that a neuron's sensitivity to interocular spatial phase disparity was reduced in the treated monkeys and that this reduction was generally more severe for units tuned to higher spatial frequencies. In the majority of the affected units, the disparity-sensitivity loss was associated with interocular differences in monocular receptive field properties. The present results suggest that the behavioral deficits in stereopsis produced by abnormal visual experience reflect at least in part the constraints imposed by alterations at the earliest stages of binocular cortical processing and support the hypothesis that the local disparity processing mechanisms in primates are spatially tuned and can be independently compromised by early abnormal visual experience.

Amblyopia↗