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视网膜退行性变大鼠的视杆细胞活性

Rod cell activity in retinal degenerative rats.

作者信息

Lue C L

机构信息

Department of Ophthalmology, College of Medicine, National Cheng Kung University, Tainan, Taiwan R.O.C.

出版信息

J Formos Med Assoc. 1994 Jul;93(7):605-10.

PMID:7866059
Abstract

The Royal College of Surgeons (RCS) rat is a good model for the study of the early onset of retinal degenerative disorders. RCS retinal disease is often associated with the loss of rhodopsin in outer segment membranes and the progressive degeneration of photoreceptor cells. This study was conducted to investigate the possible mechanisms of the loss of photoreceptor sensitivity. The electroretinographic responses were recorded in RCS and control rats, age 15, 25 and 35 days, as well as in adult control rats. The a-waves were analyzed using the Hood and Birch model of activation of photoresponse. Photoresponse latency in the RCS rats was prolonged as the disease progressed. The maximum recorded a-wave amplitudes were significantly lower for the RCS rats compared to the control rats. The sensitivity of a-waves as indicated by Ka, the semi-saturation constant, varied and depended on the age of the rats and degenerative stage of the disease. The model's time to peak response increased more than twofold as the degeneration advanced. The changes in a-waves indicate that RCS disease causes progressive impairment of the rod photoresponse. It also suggests that in addition to the phagocytic defect of the retinal pigment epithelium, the abnormal composition of the membrane lipids and the interphotoreceptor matrix and the rhodopsin loss may also cause abnormal photoresponses in RCS rats.

摘要

皇家外科学院(RCS)大鼠是研究视网膜退行性疾病早期发病的良好模型。RCS视网膜疾病通常与外段膜中视紫红质的丧失以及光感受器细胞的渐进性退化有关。本研究旨在探讨光感受器敏感性丧失的可能机制。记录了15、25和35日龄的RCS大鼠和对照大鼠以及成年对照大鼠的视网膜电图反应。使用Hood和Birch光反应激活模型分析a波。随着疾病进展,RCS大鼠的光反应潜伏期延长。与对照大鼠相比,RCS大鼠记录到的最大a波振幅显著更低。由半饱和常数Ka表示的a波敏感性各不相同,且取决于大鼠的年龄和疾病的退化阶段。随着退化进展,模型的反应峰值时间增加了两倍多。a波的变化表明RCS疾病导致视杆光反应的渐进性损害。这也表明,除了视网膜色素上皮的吞噬缺陷外,膜脂质和光感受器间基质的异常组成以及视紫红质的丧失也可能导致RCS大鼠出现异常光反应。

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