Matsuura Tetsuro, Tsuji Naho, Kodama Yasushi, Narama Isao, Ozaki Kiyokazu
Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, 45-1, Nagaotoge-cho, Hirakata, Osaka 573-0101, Japan.
Vet Ophthalmol. 2013 May;16(3):186-91. doi: 10.1111/j.1463-5224.2012.01048.x. Epub 2012 Jul 19.
Fatty liver Shionogi (FLS) mice exhibit characteristic retinochoroidal coloboma because of a failure in fusion of the embryonic optic fissure. However, the same pathogenesis should result in iridal coloboma that has not been reported in this strain. The purpose of this study was to describe the physiologic and morphometric changes in iridal tissue involved in ocular coloboma in FLS mice.
The miotic response after light exposure was evaluated in three strains of live mice, and the shape and location of the pupil were judged macroscopically. Subsequently, macroscopic abnormalities in the anterior segment and fundus were observed postmortem in all mice. During miotic and mydriatic responses in the eyes of live male FLS mice with dyscoric and normal pupils, each iris was measured in four radial directions. The enucleated eyes were examined morphometrically and histologically in both sexes of FLS mice.
Inferior corectopia upon light-induced miosis was clearly detected in live FLS mice. The deviated pupils were not round but oval-shaped. Clinical and postmortem examination revealed that all dyscoric eyes had hypoplastic and dysfunctional irides inferiorly in FLS mice. Histopathological examination confirmed that both the dilator and sphincter muscles and iris stroma were quantitatively diminished in the affected inferior iris. Meanwhile, the rate of fundus (retinochoroidal) coloboma in eyes exhibiting dyscoria was remarkably high, although some dyscoric eyes had no fundus coloboma.
Fatty liver Shionogi mice had iridal coloboma, resulting in inferior corectopia upon light-induced miosis as an indicator of ocular coloboma.
脂肪性肝Shionogi（FLS）小鼠由于胚胎视裂融合失败而表现出特征性的视网膜脉络膜缺损。然而，相同的发病机制应该会导致虹膜缺损，而该品系中尚未有相关报道。本研究的目的是描述FLS小鼠眼缺损中虹膜组织的生理和形态学变化。
在三种活体小鼠品系中评估光照后的瞳孔缩小反应，并通过肉眼判断瞳孔的形状和位置。随后，在所有小鼠死后观察眼前段和眼底的宏观异常。在患有瞳孔异常和正常瞳孔的活体雄性FLS小鼠的眼睛进行瞳孔缩小和散大反应期间，在四个径向方向测量每个虹膜。对FLS小鼠的雌雄两性摘除的眼睛进行形态学和组织学检查。
在活体FLS小鼠中明显检测到光诱导瞳孔缩小时的下方瞳孔异位。偏离的瞳孔不是圆形而是椭圆形。临床和死后检查显示，在FLS小鼠中，所有瞳孔异常的眼睛下方虹膜均发育不全且功能失调。组织病理学检查证实，受影响的下方虹膜中瞳孔开大肌和括约肌以及虹膜基质在数量上均减少。同时，表现出瞳孔异常的眼睛中眼底（视网膜脉络膜）缺损的发生率非常高，尽管一些瞳孔异常的眼睛没有眼底缺损。
脂肪性肝Shionogi小鼠存在虹膜缺损，导致光诱导瞳孔缩小时出现下方瞳孔异位，作为眼缺损的一个指标。
