Colchicine attenuates compensation to negative but not to positive lenses in young chicks

Choh, Vivian; Padmanabhan, Venkata N.; Li, W.S. Jennifer; Sullivan, Alan; Wildsoet, Christine F.

doi:10.1016/j.exer.2007.10.017

Cited by 14 publications

(8 citation statements)

References 21 publications

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“…The relative selectivity of these toxic effects may reflect the greater density of glucagonergic receptors on RPE compared with other cells in the retina and choroid [185]. Interestingly, intravitreal colchicine, which eliminates glucagonergic amacrine cells, leads to excessive eye growth in normal eyes [175], while it suppresses the ability to respond to negative lenses but leaves compensation to positive lenses relatively unchanged [186]. In normal eyes glucagon inhibits equatorial eye growth and glucagon antagonists enhance it [187].…”

Section: Glucagon Igf-1 and Insulinmentioning

confidence: 99%

Pharmaceutical intervention for myopia control

Ganesan

Wildsoet

2010

Expert Review of Ophthalmology

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Myopia is the result of a mismatch between the optical power and the length of the eye, with the latter being too long. Driving the research in this field is the need to develop myopia treatments that can limit axial elongation. When axial elongation is excessive, as in high myopia, there is an increased risk of visual impairment and blindness due to ensuing pathologies such as retinal detachments. This article covers both clinical studies involving myopic children, and studies involving animal models for myopia. Atropine, a nonselective muscarinic antagonist, has been studied most extensively in both contexts. Because it remains the only drug used in a clinical setting, it is a major focus of the first part of this article, which also covers the many shortcomings of topical ophthalmic atropine. The second part of this article focuses on in vitro and animal-based drug studies, which encompass a range of drug targets including the retina, retinal pigment epithelium and sclera. While the latter studies have contributed to a better understanding of how eye growth is regulated, no new antimyopia drug treatments have reached the clinical setting. Less conservative approaches in research, and in particular, the exploration of new bioengineering approaches for drug delivery, are needed to advance this field. Keywordsanimal models; atropine; clinical trials; dopamine; eye growth; growth factors; myopia Myopia describes the refractive error in which light entering the eye from distant objects is focused in front of the retina, leading to blurred vision. The condition is most commonly the result of excessive elongation of the posterior vitreous chamber of the eye, increasing the risk of retinal detachment and some degenerative retinal conditions, and rendering high myopia a major cause of visual impairment and blindness [1][2][3][4][5][6]. Myopia has become a major public health concern owing to rapid rises in the prevalence of myopia, first noted in East Asian populations. For example, as of the year 2000, the prevalence of myopia had reached 84% for Taiwanese adolescents between 16 and 18 years of age. Of the 18-yearolds, 21% were highly myopic, putting them at high risk for pathologic conditions in the future [7]. Similar trends are evident in recently published myopia prevalence figures for the USA, although they are not as high as East Asian figures [8][9][10][11].The management of myopia has been mostly directed at correcting the mismatch between the eye's optical power and its length using either optical means, such as single-vision spectacles and contact lenses, or refractive surgeries, such as photorefractive keratectomy (PRK) and laser-assisted in situ keratomileusis (LASIK), which both involve reshaping and thus modifying the optical power of the cornea. While these options restore sharp distance vision in myopes, they do nothing to control myopia progression. On the other hand, the © 2010 Expert Reviews Ltd † Author for correspondence: prema@berkeley.edu. NIH Public Access Author ManuscriptExpert Rev O...

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Section: Glucagon Igf-1 and Insulinmentioning

confidence: 99%

Pharmaceutical intervention for myopia control

Ganesan

Wildsoet

2010

Expert Review of Ophthalmology

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“…In particular, in chickens, colchicine, a neurotoxin, disrupts compensation to negative-lenses without producing substantial alterations in the hyperopic shifts induced by positive lenses. 22 In guinea pigs sectioning the optic nerve retards compensation for positive lenses without significantly altering the myopic changes produced by negative lenses, which suggests that extraocular mechanisms are involved in compensation for positive lenses. 23 As a consequence, it is not prudent to assume that the spatial integration properties for myopic and hyperopic defocus are the same.…”

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confidence: 99%

Effects of Local Myopic Defocus on Refractive Development in Monkeys

Smith¹,

Hung²,

Huang³

et al. 2013

Optometry and Vision Science

100

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Purpose Visual signals that produce myopia are mediated by local, regionally selective mechanisms. However, little is known about spatial integration for signals that slow eye growth. The purpose of this study was to determine whether the effects of myopic defocus are integrated in a local manner in primates. Methods Beginning at 24±2 days of age, seven rhesus monkeys were reared with monocular spectacles that produced 3 D of relative myopic defocus in the nasal visual field of the treated eye, but allowed unrestricted vision in the temporal field (NF monkeys). Seven monkeys were reared with monocular +3 D lenses that produced relative myopic defocus across the entire field of view (FF monkeys). Comparison data from previous studies were available for 11 control monkeys, 8 monkeys that experienced 3 D of hyperopic defocus in the nasal field, and 6 monkeys exposed to 3 D of hyperopic defocus across the entire field. Refractive development, corneal power, and axial dimensions were assessed at 2- to 4-week intervals using retinoscopy, keratometry, and ultrasonography, respectively. Eye shape was assessed using magnetic resonance imaging. Results In response to full-field myopic defocus, the FF monkeys developed compensating hyperopic anisometropia, the degree of which was relatively constant across the horizontal meridian. In contrast, the NF exhibited compensating hyperopic changes in refractive error that were greatest in the nasal visual field. The changes in the pattern of peripheral refractions in the NF monkeys reflected interocular differences in vitreous chamber shape. Conclusions As with form deprivation and hyperopic defocus, the effects of myopic defocus are mediated by mechanisms that integrate visual signals in a local, regionally selective manner in primates. These results are in agreement with the hypothesis that peripheral vision can influence eye shape and potentially central refractive error in a manner that is independent of central visual experience.

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“…4 This recovery can be achieved only if the chick is still in the critical phase of development, which is characterized by the capability of a high ocular growth rate, relative to adulthood. 6,9 Importantly, when the retina is disconnected from the brain experimentally, whether through optic nerve section (ONS), 10 exposure of retinal ganglion cells (RGCs) to tetrodotoxin (TTX) 11 that blocks RGC action potentials, or colchicine, 12 which selectively destroys RGCs, eyes retain the ability to respond to visual cues. 4,13 Indeed, ONS eyes are still able to respond locally to defocus or form deprivation (FD) that is confined to local retinal regions.…”

mentioning

confidence: 99%