Recovery from Form-Deprivation Myopia in Rhesus Monkeys

College of Optometry, University of Houston, Houston, Texas 77204-2020, USA.
Investigative Ophthalmology &amp Visual Science (Impact Factor: 3.4). 11/2004; 45(10):3361-72. DOI: 10.1167/iovs.04-0080
Source: PubMed


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.
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.
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.
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.

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Available from: Chea-Su Kee, Mar 25, 2014
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    • "Our experiments show that following the onset of unrestricted vision, the eye can recover from experimentally induced central and peripheral refractive errors. The results extend previous findings on the recovery of central refractive errors in infant monkeys (Qiao-Grider et al., 2004) to include the alterations in peripheral refraction that develop in concert with central refractive errors. Consistent with previous observations that vision-induced alterations in peripheral refractions reflect corresponding alterations in ocular shape (Huang et al., 2009), our experiments indicate that the recovery of peripheral refraction is also associated with changes in the shape of the posterior globe. "
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    ABSTRACT: This study aimed to investigate the changes in ocular shape and relative peripheral refraction during the recovery from myopia produced by form deprivation (FD) and hyperopic defocus. FD was imposed in six monkeys by securing a diffuser lens over one eye; hyperopic defocus was produced in another six monkeys by fitting one eye with -3D spectacle. When unrestricted vision was re-established, the treated eyes recovered from the vision-induced central and peripheral refractive errors. The recovery of peripheral refractive errors was associated with corresponding changes in the shape of the posterior globe. The results suggest that vision can actively regulate ocular shape and the development of central and peripheral refractions in infant primates.
    Vision research 09/2012; 73C:30-39. DOI:10.1016/j.visres.2012.09.002 · 1.82 Impact Factor
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    • "Guinea pigs are a promising alternative to chickens and other mammals for the study of experimental myopia [34,53-56]. They develop myopia more rapidly compared to monkeys [57-59] and have shown that local DA signaling plays a significant role in inhibition of form deprivation myopia [5,6,60]. "
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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. · 1.99 Impact Factor
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    • "In placental mammals and primates, the rate of vitreous chamber elongation is inversely related to the rate of proteoglycan synthesis in the posterior sclera (McBrien et al., 2000; Moring et al., 2007; Norton and Rada, 1995; Rada et al., 2000; Troilo et al., 2006) while in the chick, increased axial elongation and development of myopia are associated with significant increases in proteoglycan synthesis in the cartilaginous layer of the sclera (Christensen and Wallman, 1991; Gentle et al., 2001; Marzani and Wallman, 1997; McBrien et al., 1991; Rada et al., 1991, 1994). In both chicks and primates, visually induced changes in ocular elongation and sclera proteoglycan synthesis are reversible; restoration of unrestricted vision (and the resultant myopia) results in a temporary cessation of axial growth, eventually leading to re-establishment of emmetropia ( " recovery " ) in the formerly deprived eye (McBrien et al., 2000; Siegwart and Norton, 1998; Qiao-Grider, et al., 2004; Rada et al., 1992; Wallman and Adams, 1987). Moreover, the ocular response to FD or defocus is rapid, leading to detectible changes in vitreous chamber depth within hours (Winawer and Wallman, 2005). "
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    ABSTRACT: During the recovery from form deprivation myopia (myopic defocus), the rate of proteoglycan synthesis in the posterior sclera decreases co-incident with a deceleration of axial elongation. The choroid has been implicated in the regulation of scleral proteoglycan synthesis, possibly through the synthesis and secretion of scleral growth inhibitors. Therefore these studies were carried out to attempt to establish a causal relationship between choroidal secretion and the inhibition of scleral proteoglycan synthesis during the recovery from induced myopia. Chicks were form vision deprived for 10 days followed by a recovery period (3 h-20 days) of unrestricted vision. Sclera and choroids (5 mm punches) were isolated from control and treated eyes. The rate of proteoglycan synthesis was estimated by the incorporation of (3)(5)c in cetylpyridinium chloride-precipitable glycosaminoglycans by isolated sclera of control and treated eyes. Additionally, choroids from control and treated eyes were placed in co-culture with untreated age-matched normal chick sclera for 20-24 h, after which time sclera were removed and scleral proteoglycan synthesis rates were determined. Following removal of occluders, a biphasic decline was observed in scleral proteoglycan synthesis: A rapid decline in proteoglycan synthesis (-7.6% per hr; r(2) = 0.923) was observed over the first 12 h of recovery, followed by a slow decline extending from 12 to 96 h (-0.3% per hr; r(2) = 0.735). Proteoglycan synthesis rates gradually increased to control levels over the next 96 h at a rate of +0.3% per hr. No relative proteoglycan inhibition was observed when untreated sclera were co-cultured with choroids from eyes recovering for 0-4 days, whereas co-culture of untreated sclera with choroids from eyes recovering for 5 and 8 days resulted in significant inhibition of sclera proteoglycan synthesis, relative to that of sclera co-cultured with choroids from control eyes (≈-24%, P < 0.05, paired t-test). In conclusion, recovery from induced myopia is characterized by a rapid decline in proteoglycan synthesis which occurs within the first 12 h of unrestricted vision as a well as a slower more gradual decline that occurs over the next four days. Choroidal inhibition of scleral proteoglycan synthesis in vitro occurs during the second phase of decline and is most likely related to increased choroidal permeability; whereas the rapid decline in proteoglycan synthesis that occurs during the first 12 h of recovery is regulated by an independent, yet to be identified mechanism.
    Experimental Eye Research 02/2011; 92(5):394-400. DOI:10.1016/j.exer.2011.02.011 · 2.71 Impact Factor
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