Teramoto Y, Uga S, Matsushima Y, Shimizu K, Morita T, Shirakawa S
Department of Ophthalmic Anatomy and Physiology, Graduate School of Medical Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan.
Graefes Arch Clin Exp Ophthalmol. 2000 Dec;238(12):970-8. doi: 10.1007/s004170000190.
To clarify the causative factor underlying rupture of the posterior capsule of the RLC mouse lens as a recessive trait around the 50th postnatal day.
The lenses of the RLC mouse were removed in the period from birth to 50th postnatal day. Some specimens were observed by light microscopy and transmission and scanning electron microscopy. Others were examined as flat preparations of the lens epithelium.
There was an abnormal arrangement of lens fibers at the newborn stage, and lens fibers of the perinuclear zone ended almost vertical in relation to the posterior capsule. Consequently, the posterior suture was not formed in this mouse lens. On the 10th postnatal day, the ends of the lens fibers that terminated in the posterior capsule became swollen, and the posterior capsule at the posterior polar region became thin. On the 20th day, the area of swollen fibers was so large at the center of the posterior capsule that a vacuolated area was observed under the dissecting microscope. On the 30th day, the posterior cortical fibers in this area showed marked swelling, and the posterior capsule became extremely thin. On the 40th day, the anterior cortex became unusually thick, and the lens nucleus was dislocated towards the posterior capsule. On the 50th day, the posterior capsule ruptured. At this time the lens fibers from the perinuclear zone constituted the central area of rupture, and the cortical fibers from the equator formed the protruded area outside the lens.
The findings revealed that the RLC mouse lens has an abnormal lens fiber arrangement from the early period of lens development, that the lens fibers from the perinuclear zone cause swelling without forming the posterior suture, and that the thin capsule is ruptured by pushing out of the nucleus by thickening of the anterior cortex.
阐明RLC小鼠晶状体后囊破裂作为一种隐性性状在出生后第50天左右的潜在致病因素。
在出生至出生后第50天期间摘除RLC小鼠的晶状体。部分标本通过光学显微镜、透射电子显微镜和扫描电子显微镜观察。其他标本作为晶状体上皮的平铺标本进行检查。
在新生阶段晶状体纤维排列异常,核周区的晶状体纤维相对于后囊几乎垂直终止。因此,该小鼠晶状体未形成后缝线。出生后第10天,终止于后囊的晶状体纤维末端肿胀,后极区的后囊变薄。第20天,后囊中央肿胀纤维区域很大,在解剖显微镜下可观察到一个空泡化区域。第30天,该区域的后皮质纤维明显肿胀,后囊变得极薄。第40天,前皮质异常增厚,晶状体核向后囊移位。第50天,后囊破裂。此时,来自核周区的晶状体纤维构成破裂的中央区域,来自赤道的皮质纤维形成晶状体外部的突出区域。
研究结果表明,RLC小鼠晶状体从晶状体发育早期就存在异常的晶状体纤维排列,核周区的晶状体纤维在不形成后缝线的情况下发生肿胀,薄的囊膜因前皮质增厚导致核突出而破裂。