Smith EL III, Hung LF, Kee CS, Qiao Y. Effects of brief periods of unrestricted vision on the development of form-deprivation myopia in monkeys

College of Optometry, University of Houston, Houston, Texas 77204-2020, USA.
Investigative Ophthalmology &amp Visual Science (Impact Factor: 3.66). 03/2002; 43(2):291-9.
Source: PubMed

ABSTRACT To characterize the temporal integration properties of the mechanisms responsible for form-deprivation myopia (FDM), the effects of brief daily periods of unrestricted vision on the degree of FDM were investigated in infant monkeys.
Starting at approximately 3 weeks of age, unilateral form deprivation was produced in 24 infant rhesus monkeys by securing a diffuser spectacle lens in front of one eye and a clear, zero-powered lens in front of the fellow eye. During the treatment period (17 +/- 2 weeks), six infants wore the diffuser lenses continuously. In the other experimental infants, the diffuser lenses were removed each day and replaced with clear, zero-powered lenses for 1 (n = 7), 2 (n = 7), or 4 hours (n = 4). Refractive development was assessed by retinoscopy and A-scan ultrasonography. Control data were obtained from 11 normal infants and 3 infants reared with zero-powered lenses over both eyes.
The degree of FDM varied significantly with the duration of unrestricted vision. Continuous form deprivation produced -5.2 +/- 3.6 D of relative axial myopia. However, 1 hour of unrestricted vision was sufficient to reduce the degree of axial FDM by more than 50% (-1.7 +/- 3.2 D). The infants that were allowed 4 hours of unrestricted vision exhibited only -0.4 +/- 0.5 D of FDM.
As observed in chickens and tree shrews, relatively long periods of form deprivation can be counterbalanced by quite short periods of unrestricted vision. These results indicate that the processes or signals that promote axial elongation in monkeys are comparatively weak or easily overridden by factors that slow ocular growth.

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Available from: Chea-Su Kee, Mar 25, 2014
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    • "However, it should be noted that the magnitudes of changes at corresponding areas were quite similar within 30° eccentricities (Figs. 3 and 4), suggesting that the effects of asymmetric eye movement or eye's fixating behavior, if there is any, should be minimal. Nevertheless, given the facts that chicks could exert 10–20° lateral eye movements (Schippert & Schaeffel, 2006), and that only brief periods of unrestricted vision could significantly attenuate the effects of form-deprivation or defocus-induced myopia (Kee et al., 2007; Napper et al., 1997; Shaikh, Siegwart, & Norton, 1999; Smith et al., 2002; Winawer & Wallman, 2002), it is possible that had we covered more than half of the retina, like those device used by Wallman and coworkers (1987), the changes in central ametropia and ocular dimensions would have been larger . In this respect, previous studies using occluders (Stone et al., 2006) or spherical lenses (Morgan & Ambadeniya, 2006; Schippert & Schaeffel, 2006) with central aperture (i.e., unrestricted central visual field) have consistently shown that central ametropia can be induced only if the size of the peripheral visual deprivations was big enough to cover a critical region around the central retina in chicks (see also Irving et al., 1995), our results provide further evidence that even if the central retina in the treated chicks might have been partially exposed to unrestricted vision, covering the four hemi-retinal sectors can still produce different impacts on central ametropia (Fig. 2). "
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    ABSTRACT: We determined effects of hemiretinal form deprivation (i.e., form-depriving half of the retina) on central refractive development and posterior eye shape in chicks. Seventy-seven White Leghorn chicks were randomly assigned to receive superior (SRD, "Superior Retinal Deprivation" or inferior visual field deprivation, same principle applies for the following abbreviations, n=17), inferior (IRD, n=14), temporal (TRD, n=23) or nasal hemiretinal (NRD, n=23) form deprivation monocularly from day 5 to day 26. Central refractive errors, expressed as interocular difference in spherical equivalent (M), J0 and J45 astigmatic components, were measured using Hartinger refractometer at the beginning and weekly after treatment for 3weeks. At the end of the treatment period, eyes of a subset of birds were enucleated and eye shape profile was photographed along four different meridians. These digital images were later processed to extract axial length (AL), equatorial diameter (ED), and AL/ED. For comparison purposes, the eye shape profile was also acquired from a separate group of birds reared with monocular full-retinal form deprivation (FRD, n=10). The four hemiretinal form deprivations altered central ametropia and posterior eye shape to different degrees. The biggest contrast in M was found between SRD and IRD groups (mean±SE after 3weeks: SRD=-4.14±0.71 D vs. IRD=+1.24±0.36 D; p<0.05), whereas subtle differences in J0 and J45 components were found across the four treatment groups (both p⩽0.03). SRD group also showed significantly higher AL/ED ratio compared to IRD and NRD groups (0.76±0.05 vs. 0.74±0.07 and 0.75±0.04; both p⩽0.03). Furthermore, M was significantly correlated with AL/ED ratio in the treated eyes of hemiretinal treated chicks (r=-0.55, p<0.001). Our results suggest that mechanism regulating central ametropia can be influenced by selectively interrupting the visual experience at different parts of visual field.
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    • "An understanding of DA involved in the development of myopia could help select potential medical treatment for refractive errors. At present, neurochemical mechanisms involved in myopia development have not been studied as extensively in mammals as in chickens although studies on monkeys and tree shrews have provided some results similar to those in chickens [51,52]. Guinea pigs are a promising alternative to chickens and other mammals for the study of experimental myopia [34,53-56]. "
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    ABSTRACT: The dopamine (DA) system in the retina is critical to normal visual development as lack of retinal DA signaling may contribute to myopic development. The involvement of DA in myopic development is complex and may be different between form deprivation and hyperopic defocus. This study evaluated effects of a non-selective DA receptor agonist, apomorphine (APO) on refractive development in guinea pigs treated with form deprivation or hyperopic defocus. APO was subconjunctivally injected daily for 11 days in form-deprived (0.025 to 2.5 ng/µl) and defocused (0.025 to 250 ng/µl) eyes. Changes in ocular biometry and retinal concentration of DA and its metabolites (DOPAC) were measured in the 2 animal models to assess the level of DA involvement in each of the models (the less the change, the lower the involvement). Similar myopic degree was induced in both the deprived and defocused eyes (-4.06 D versus -3.64 D) at 11 days of the experiment. DA and DOPAC levels were reduced in the deprived eyes but did not change significantly in the defocused eyes compared to the fellow and normal control eyes. A subconjunctival injection of APO daily for 11 days at concentrations ranged from 0.025 to 2.5 ng/µl inhibited form deprivation myopia in a concentration-dependent manner. By contrast, the APO treatment ranged from 0.025 to 250 ng/µl did not effectively inhibit the defocus-induced myopia and the associated axial elongation. DA signaling may play a more critical role in form deprivation myopia than in defocus-induced myopia, raising a question whether the mechanisms of DA signaling are different under these two types of experimental myopia.
    Molecular vision 10/2011; 17:2824-34. · 2.25 Impact Factor
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    • "In particular, in a wide variety of animal species, experimentally induced refractive errors are associated with alterations in vitreous chamber depth and axial length. For example, myopia produced by form deprivation or optical defocus is associated with vitreous chamber elongation in chicks (Schaeffel et al., 1988; Wallman & Adams, 1987; Wildsoet & Wallman, 1995), tree shrews (Marsh-Tootle & Norton, 1989; McBrien & Norton, 1992; Norton et al., 2006), guinea pigs (Howlett & McFadden, 2006; Jiang et al., 2009), marmosets (Graham & Judge, 1999; Troilo & Judge, 1993), and macaques (Greene, 1990; Hung et al., 1995; Qiao-Grider et al., 2004; Smith et al., 1999a; Smith et al., 1987; Smith & Hung, 2000; Smith et al., 2002a; Tigges et al., 1990; Wiesel & Raviola, 1977). However, the associations between experimental refractive errors and other ocular component changes are less consistent between species and, in some cases, between studies. "
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    ABSTRACT: 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.
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