Experimental myopia in tree shrews.

T. Norton
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引用次数: 105

Abstract

When deprived of form vision during postnatal development, tree shrews reliably develop an axial myopia characterized by elongation of the vitreous chamber, zonular dysplasia and a slight reduction in lens weight and thickness. Corneal flattening has been observed in animals visually deprived by eyelid suture but is absent in animals visually deprived with an opaque goggle. The sensitive period for myopia development starts about 15 days after the eyes open and sensitivity remains high for about 3-4 weeks thereafter. Recovery from experimental myopia can occur in tree shrews that are visually deprived using goggles for a short period. Blockade of action potentials from ganglion cells in deprived eyes by intravitreal injections of tetrodotoxin (TTX) does not prevent the development of myopia, suggesting that local retinoscleral mechanisms can contribute to experimental myopia in this species. Open eyes receiving intravitreal injections of either saline or TTX have shorter vitreous chambers than control eyes, suggesting that puncturing the globe reduces forces within the eye that contribute to its expansion. Animals treated intraperitoneally with lathyritic agents to block collagen cross-linking for three weeks during a 75-day period of monocular visual deprivation develop a very large myopia in the visually deprived eye that is accompanied by a large vitreous chamber elongation and marked thinning of the posterior sclera. The results from studies in tree shrews are consistent with the suggestion that an internally driven expansion acts in concert with ocular growth to increase the axial length of the eye, helping to move the eye from hyperopia toward emmetropia. The resistance of the sclera and/or choroid to this expansion may be affected by activity within the retina. Increased retinal activity associated with achieving a clear image on the retina may result in increased resistance to expansion, helping to hold the retina at the focal plane. Recovery may occur by a slowing of axial expansion while the optical surfaces proceed toward adult values.
树鼩的实验性近视。
在出生后的发育过程中,当被剥夺视觉时,树鼩必然会发展为轴向近视,其特征是玻璃体腔延长,带状发育不良和晶状体重量和厚度轻微减少。在眼睑缝合剥夺视力的动物中观察到角膜变平,但在使用不透明护目镜剥夺视力的动物中没有角膜变平。近视发展的敏感期开始于睁眼后约15天,此后约3-4周内敏感性保持高水平。在短时间内使用护目镜剥夺视觉的树鼩可以从实验性近视中恢复过来。通过玻璃体内注射河豚毒素(TTX)阻断被剥夺眼睛的神经节细胞的动作电位并不能阻止近视的发展,这表明局部视网膜巩膜机制可能有助于该物种的实验性近视。接受玻璃体内生理盐水或TTX注射的裸眼玻璃体腔比对照组的眼睛短,这表明刺穿眼球会减少眼内促进其扩张的力量。在75天的单眼视力剥夺期间,腹腔注射溶石剂阻断胶原交联三周的动物会在视力剥夺的眼睛中出现非常大的近视,并伴有玻璃体腔的大延伸和后巩膜的明显变薄。对树鼩的研究结果与内部驱动的扩张与眼部生长相一致,以增加眼睛的轴向长度,帮助眼睛从远视转向远视。巩膜和/或脉络膜对这种扩张的抵抗力可能受到视网膜内活动的影响。在视网膜上获得清晰图像的视网膜活动增加可能导致对扩张的阻力增加,有助于将视网膜保持在焦平面上。当光学表面向成体值方向发展时,轴向扩张的减慢可能会导致恢复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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