The refractive development of untreated eyes of rhesus monkeys varies according to the treatment received by their fellow eyes.
(9/757)
To determine the extent to which the visual experience of one eye may influence the refractive development of its fellow eye, we analyzed the data of untreated (UT) eyes of monkeys that received different types of unilateral pattern deprivation. Subjects were 15 juvenile rhesus monkeys, with five monkeys in each of three treatment groups: aphakic eyes with optical correction (AC), aphakic eyes with no correction (ANC), and eyes that were occluded with an opaque contact lens (OC). Under general anaesthesia, refractive error (D) was determined by cycloplegic retinoscopy and axial length (mm) was determined with A-scan ultrasonography. For measurements of refractive error of the UT eyes, there was a significant main effect of groups according to the treatment of the fellow eyes, F(2, 12) = 6.6. While UT eyes paired with AC fellow eyes (mean = +4.2 D) were significantly more hyperopic than the eyes of age-matched normal monkeys (mean = +2.4 D), t(25), = 2.5, UT eyes paired with OC fellow eyes (mean = -0.5 D) were significantly more myopic than the eyes of normal monkeys, t(25) = -9. UT eyes paired with ANC fellow eyes (mean = +1.9 D) were not significantly different from normal eyes. For measurements of axial length there was also a significant main effect of groups, F(2, 12) = 6.9. While UT eyes paired with AC fellow eyes (mean = 16.9 mm) were significantly shorter than the eyes of age-matched normal monkeys (mean = 17.5 mm), t(25) = 2.3, UT eyes paired with OC fellow eyes (mean = 18.1 mm) were significantly longer than the eyes of normal monkeys, t(25) = 2.3. UT eyes paired with ANC fellow eyes (mean = 17.5 mm) were not significantly different from the eyes of normal monkeys. The measurements of axial length and of refractive error of the UT eyes were also significantly correlated with one another, probably indicating that the differences in refractive error were due to differences in axial length, r = -0.8. The present data reveal that despite normal visual experience, UT eyes can have their refractive development altered, systematically, simply as a function of the type of pattern deprivation received by their fellow eyes. These data add to the growing evidence that there is an interocular mechanism that is active during emmetropization. As a consequence, future models of eye growth will need to consider both: (1) the direct influence of visual input on the growing eye; as well as (2) the indirect influence coming from the fellow eye. (+info)
Long-term changes in retinal contrast sensitivity in chicks from frosted occluders and drugs: relations to myopia?
(10/757)
Experiments in animal models have shown that the retinal analyzes the image to identify the position of the plane of focus and fine-tunes the growth of the underlying sclera. It is fundamental to the understanding of the development of refractive errors to know which image features are processed. Since the position of the image plane fluctuates continuously with accommodative status and viewing distance, a meaningful control of refractive development can only occur by an averaging procedure with a long time constant. As a candidate for a retinal signal for enhanced eye growth and myopia we propose the level of contrast adaptation which varies with the average amount of defocus. Using a behavioural paradigm, we have found in chickens (1) that contrast adaptation (CA, here referred to as an increase in contrast sensitivity) occurs at low spatial frequencies (0.2 cyc/deg) already after 1.5 h of wearing frosted goggles which cause deprivation myopia, (2) that CA also occurs with negative lenses (-7.4D) and positive lenses (+6.9D) after 1.5 h, at least if accommodation is paralyzed and, (3) that CA occurs at a retinal level or has, at least, a retinal component. Furthermore, we have studied the effects of atropine and reserpine, which both suppress myopia development, on CA. Quisqualate, which causes retinal degeneration but leaves emmetropization functional, was also tested. We found that both atropine and reserpine increase contrast sensitivity to a level where no further CA could be induced by frosted goggles. Quisqualate increased only the variability of refractive development and of contrast sensitivity. Taken together, CA occurring during extended periods of defocus is a possible candidate for a retinal error signal for myopia development. However, the situation is complicated by the fact that there must be a second image processing mode generating a powerful inhibitory growth signal if the image is in front of the retina, even with poor images (Diether, S., & Schaeffel, F. (1999). (+info)
The critical period for ocular dominance plasticity in the Ferret's visual cortex.
(11/757)
Microelectrode recordings and optical imaging of intrinsic signals were used to define the critical period for susceptibility to monocular deprivation (MD) in the primary visual cortex of the ferret. Ferrets were monocularly deprived for 2, 7 or >14 d, beginning between postnatal day 19 (P19) and P110. The responses of visual cortical neurons to stimulation of the two eyes were used to gauge the onset, peak, and decline of the critical period. MDs ending before P32 produced little or no loss of response to the deprived eye. MDs of 7 d or more beginning around P42 produced the greatest effects. A rapid decline in cortical susceptibility to MD was observed after the seventh week of life, such that MDs beginning between P50 and P65 were approximately half as effective as those beginning on P42; MDs beginning after P100 did not reduce the response to the deprived eye below that to the nondeprived eye. At all ages, 2 d deprivations were 55-85% as effective as 7 d of MD. Maps of intrinsic optical responses from the deprived eye were weaker and less well tuned for orientation than those from the nondeprived eye, with the weakest maps seen in the hemisphere ipsilateral to the deprived eye. Analysis of the effects of 7 d and longer deprivations revealed a second period of plasticity in cortical responses in which MD induced an effect like that of strabismus. After P70, MD caused a marked loss of binocular responses with little or no overall loss of response to the deprived eye. The critical period measured here is compared to other features of development in ferret and cat. (+info)
Asymmetric responses in cortical visually evoked potentials to motion are not derived from eye movements.
(12/757)
PURPOSE: Normal neonates and many adults after abnormal visual development have directional preferences for visual stimulus motions; i.e., they give better responses for optokinetic nystagmus (OKN) and visually evoked potentials (VEPs) in one direction than to those in the opposite direction. The authors tested whether the VEP responses were asymmetrical because of abnormal eye movements. METHODS: VEPs were recorded from the visual cortices of five macaque monkeys: one normal, one neonate, and three reared with alternating monocular occlusion (AMO). They were lightly anesthetized, followed by paralysis to prevent eye movements. They then had "jittered" vertical grating patterns presented in their visual fields. The steady state VEPs were analyzed with discrete Fourier transforms to obtain the amplitudes and phases of the asymmetries. RESULTS: The normal, control monkey had small, insignificant amplitudes of its asymmetrical Fourier component and random phases that were not 180 degrees out of phase across the left and right eyes. The neonatal monkey and the AMO monkeys all had large, significant asymmetries that were approximately 180 degrees out of phase between the left and right eyes. CONCLUSIONS: The neonate and abnormally reared monkeys continued to have asymmetrical responses even after their eyes were paralyzed. Therefore, eye movements cannot be the source of the asymmetrical amplitudes of the VEPs, and the visual cortex is at least one source responsible for asymmetries observed in neonates and adults reared under abnormal visual inputs. (+info)
Functional visual loss in amblyopia and the effect of occlusion therapy.
(13/757)
PURPOSE: The aim of this study was to define the nature of functional visual loss in amblyopia and to identify those subjects whose amblyopia is chiefly due to one or more of the following deficits: abnormal contour interaction, abnormal eye movements, abnormal contrast perception, or positional uncertainty. METHODS: Fifty amblyopic children with a mean age of 5.6+/-1.3 years were referred from diverse sources. In addition to routine orthoptic and optometric evaluation the principal visual deficits in the amblyopic eye of each subject were identified using the following measures of visual acuity: high contrast linear, single optotype, repeat letter and low contrast linear, plus Vernier and displacement thresholds. These measures were repeated as the children underwent a prescribed occlusion therapy regime, after parental consent. RESULTS: All amblyopic subjects demonstrated a functional loss in each of the tests used, and occlusion therapy appeared to improve all aspects of the amblyopia. High contrast visual acuity was not always the primary deficit in visual function, and when amblyopic subjects were divided according to their primary visual loss, this visual function was found to show the greatest improvement with treatment. CONCLUSIONS: These results suggest that to successfully identify the primary visual deficit and monitor the success of occlusion therapy it is necessary to assess other aspects of visual function in amblyopia. (+info)
Development of receptive fields in rabbit visual cortex: changes in time course due to delayed eye-opening.
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Rabbit pups had one eye sutured closed before the time at which the eyes normally open. At 20-27 days of age, single-unit recordings were made both from the striate cortex contralateral to the sutured eye (deprived cortex) and from that contralateral to the eye which had opened normally (control cortex). The percentages of units encountered which fell into various receptive field categories differed on the two sides. The deprived cortices had a lower percentage of visually responsive cells, a higher percentage of indefinite cells, and totally lacked cells sensitive to orientation of a stimulus bar. In these respects they closely resembled previous observations on rabbit pups just before normal eye-opening. By contrast, the control cortices of the same animals were comparable to normally reared rabbits of the same age. We conclude, therefore, that developmental events which normally follow eye-opening can be affected in their time course by delaying eye-opening. (+info)
Gelatinase A and TIMP-2 expression in the fibrous sclera of myopic and recovering chick eyes.
(15/757)
PURPOSE: Myopia, or nearsightedness, is characterized by excessive lengthening of the ocular globe and is associated with extracellular matrix remodeling in the posterior sclera. The activity of gelatinase A, a member of the matrix metalloproteinase family, has been shown to increase in the posterior sclera during the development of induced myopia in several species. In the present study, the distribution and relative expression of gelatinase A and its associated inhibitor, tissue inhibitor of metalloproteinases (TIMP)-2, were measured within the fibrous scleras of experimentally myopic (form-deprived) eyes, control eyes, and eyes recovering from form deprivation to better understand the mechanisms that regulate scleral remodeling and the rate of ocular elongation. METHODS: Total RNA was extracted from the posterior scleras of form-deprived chick eyes, eyes recovering from deprivation myopia, and paired contralateral control eyes, and subjected to northern blot analysis analyses using cDNA probes to chicken gelatinase A and TIMP-2. The distribution of gelatinase A and TIMP-2 mRNAs was evaluated by in situ hybridization on frozen sections of chick scleras using 33P-labeled RNA probes. Gelatinase A activity within the fibrous scleras of form-deprived eyes and paired contralateral recovering eyes was evaluated by gelatin zymography. RESULTS: Northern blot analysis indicated that the relative expression of gelatinase A was increased by 128% in deprived eyes (P = 0.009), whereas after 1 day of recovery, levels were decreased by 80% in scleras from recovering eyes (P = 0.005). In contrast, TIMP-2 expression was significantly decreased (-53%, P = 0.027) in the posterior scleras of form-deprived eyes. No significant differences were detected in levels of TIMP-2 expression between recovering eyes and paired control eyes. In situ hybridization indicated that most of the gelatinase A transcripts were present in the fibrous layer of the posterior scleras from form-deprived and recovering eyes. CONCLUSIONS: Changes in the steady state levels of gelatinase A and TIMP-2 mRNA lead to changes in gelatinase activity within the fibrous sclera and mediate, at least in part, the process of visually regulated ocular growth and scleral remodeling. (+info)
Synaptic density in geniculocortical afferents remains constant after monocular deprivation in the cat.
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Monocular eyelid closure in cats during a critical period in development produces both physiological plasticity, as indicated by a loss of responsiveness of primary visual cortical neurons to deprived eye stimulation, and morphological plasticity, as demonstrated by a decrease in the total length of individual geniculocortical arbors representing the deprived eye. Although the physiological plasticity appears maximal after 2 d of monocular deprivation (MD), the shrinkage of deprived-eye geniculocortical arbors is less than half-maximal at 4 d and is not maximal until 7 d of deprivation, at which time the deprived arbors are approximately half their previous size. To study this form of plasticity at the level of individual thalamocortical synapses rather than arbors, we developed a new double-label colocalization technique. First, geniculocortical afferent arbors serving either the deprived or nondeprived eye were labeled by injection of the anterograde tracer Phaseolus vulgaris leucoagglutinin into lamina A of the lateral geniculate nucleus. Then, using antibodies to synaptic vesicle proteins, we identified presynaptic terminals within the labeled arbors in layer IV of the primary visual cortex. Analysis of serial optical sections obtained using confocal microscopy allowed measurement of the numerical density of presynaptic sites and the relative amounts of synaptic vesicle protein in geniculocortical afferents after both 2 and 7 d of MD. We found that the density of synapses in geniculocortical axons was similar for deprived and nondeprived afferents, suggesting that this feature of the afferents is conserved even during periods in which synapse number is reduced by half in deprived-eye arbors. These results are not consistent with the hypothesis that a rapid loss of deprived-eye geniculocortical presynaptic sites is responsible for the prompt physiological effects of MD. (+info)