Effects of Foveal Ablation on the Pattern of Peripheral Refractive Errors in Normal and Form-deprived Infant Rhesus Monkeys (<i>Macaca mulatta</i>)

Huang, Juan; Hung, Li-Fang; Smith, Earl L.

doi:10.1167/iovs.10-6757

Cited by 38 publications

(35 citation statements)

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“…The mechanisms by which the peripheral retina is involved in control of overall eye growth and refractive development have been investigated in chick, tree shrew, marmoset, and rhesus macaque (Zhu et al, 2013). We note that in experimental ametropia, peripheral defocus or deprivation has significant effect on eye shape and refractive error, whereas foveal vision is not essential for refractive development (Huang et al, 2011; Smith, 2011; Smith et al, 2014). Therefore, the abnormal foveal structure in severe ROP (Fig.…”

Section: Summary and Future Directionsmentioning

confidence: 74%

The neural retina in retinopathy of prematurity

Hansen

Moskowitz

Akula

et al. 2017

Progress in Retinal and Eye Research

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Retinopathy of prematurity (ROP) is a neurovascular disease that affects prematurely born infants and is known to have significant long term effects on vision. We conducted the studies described herein not only to learn more about vision but also about the pathogenesis of ROP. The coincidence of ROP onset and rapid developmental elongation of the rod photoreceptor outer segments motivated us to consider the role of the rods in this disease. We used noninvasive electroretinographic (ERG), psychophysical, and retinal imaging procedures to study the function and structure of the neurosensory retina. Rod photoreceptor and post-receptor responses are significantly altered years after the preterm days during which ROP is an active disease. The alterations include persistent rod dysfunction, and evidence of compensatory remodeling of the post-receptor retina is found in ERG responses to full-field stimuli and in psychophysical thresholds that probe small retinal regions. In the central retina, both Mild and Severe ROP delay maturation of parafoveal scotopic thresholds and are associated with attenuation of cone mediated multifocal ERG responses, significant thickening of post-receptor retinal laminae, and dysmorphic cone photoreceptors. These results have implications for vision and control of eye growth and refractive development and suggest future research directions. These results also lead to a proposal for noninvasive management using light that may add to the currently invasive therapeutic armamentarium against ROP.

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Section: Summary and Future Directionsmentioning

confidence: 74%

The neural retina in retinopathy of prematurity

Hansen

Moskowitz

Akula

et al. 2017

Progress in Retinal and Eye Research

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“…It is well established that information important for emmetropization is communicated directly to the sclera via a signaling cascade involving retinal pigment epithelium, choroid and sclera (Guo et al, 2013; Guo et al, 2014; He et al, 2014a, b). This direct, spatially-local pathway is able to separately modulate emmetropization in the central or peripheral visual fields and produce emmetropia (albeit less effectively) if communication through the optic nerve is severed (Huang et al, 2011; Norton and Siegwart, 1991; Norton et al, 1994; Smith et al, 2007; Wildsoet and McFadden, 2010). Whatever the retinal mechanisms that guide emmetropization through this direct retina-RPE-choroid-sclera signaling pathway, they likely have access to information about high temporal frequencies at short wavelengths.…”

Section: Discussionmentioning

confidence: 99%

The wavelength composition and temporal modulation of ambient lighting strongly affect refractive development in young tree shrews

Gawne

Siegwart

Ward

et al. 2017

Experimental Eye Research

105

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Shortly after birth, the eyes of most animals (including humans) are hyperopic because the short axial length places the retina in front of the focal plane. During postnatal development, an emmetropization mechanism uses cues related to refractive error to modulate the growth of the eye, moving the retina toward the focal plane. One possible cue may be longitudinal chromatic aberration (LCA), to signal if eyes are getting too long (long [red] wavelengths in better focus than short [blue]) or too short (short wavelengths in better focus). It could be difficult for the short-wavelength sensitive (SWS, “blue”) cones, which are scarce and widely spaced across the retina, to detect and signal defocus of short wavelengths. We hypothesized that the SWS cone retinal pathway could instead utilize temporal (flicker) information. We thus tested if exposure solely to long-wavelength light would cause developing eyes to slow their axial growth and remain refractively hyperopic, and if flickering short-wavelength light would cause eyes to accelerate their axial growth and become myopic. Four groups of infant northern tree shrews (Tupaia glis belangeri, dichromatic mammals closely related to primates) began 13 days of wavelength treatment starting at 11 days of visual experience (DVE). Ambient lighting was provided by an array of either long-wavelength (red, 626±10 nm) or short-wavelength (blue, 464±10 nm) light-emitting diodes placed atop the cage. The lights were either steady, or flickering in a pseudo-random step pattern. The approximate mean illuminance (in human lux) on the cage floor was red (steady, 527 lux; flickering, 329 lux), and blue (steady, 601 lux; flickering, 252 lux). Refractive state and ocular component dimensions were measured and compared with a group of age-matched normal animals (n=15 for refraction (first and last days); 7 for ocular components) raised in broad spectrum white fluorescent colony lighting (100-300 lux). During the 13 day period, the refraction of the normal animals decreased from (mean±SEM) 5.8±0.7 diopters (D) to 1.5±0.2 D as their vitreous chamber depth increased from 2.77±0.01mm to 2.80±0.03 mm. Animals exposed to red light (both steady and flickering) remained hyperopic throughout the treatment period so that the eyes at the end of wavelength treatment were significantly hyperopic (7.0±0.7 D, steady; 4.7±0.8 D, flickering) compared with the normal animals (p<0.01). The vitreous chamber of the steady red group (2.65±0.03 mm) was significantly shorter than normal (p<0.01). On average, steady blue light had little effect; the refractions paralleled the normal refractive decrease. In contrast, animals housed in flickering blue light increased the rate of refractive decrease so that the eyes became significantly myopic (−2.9±1.3 D) compared with the normal eyes and had longer vitreous chambers (2.93±0.04 mm). Upon return to colony lighting, refractions in all groups gradually returned toward emmetropia. These data are consistent both with the hypothesis that LCA can be an important visual...

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“…Thus, there is an assumption that cone pathways likely underlie the signaling needed for proper eye growth control. However, results from a few studies suggest that cone pathways may not dominate the signaling of mammalian eye growth: (1) Laser ablation of the cone-rich fovea region in monkeys did not prevent the development of FD myopia 13,14 and (2) imposing FD on the rod-dominated peripheral regions of the monkey eye produced similar magnitudes of FD myopia as when the entire visual field was affected. 15 The limitation of these studies is that rods and cones are present in the periphery of the retina and, thus, a small population of cones still could be contributing signals for eye growth.…”

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confidence: 99%