Raz Dorit, Perlman Ido, Percicot Christine L, Lambrou George N, Ofri Ron
Koret School of Veterinary Medicine, Hebrew University of Jerusalem, Rehovot, Israel.
Invest Ophthalmol Vis Sci. 2003 Aug;44(8):3675-84. doi: 10.1167/iovs.02-1236.
To investigate the cellular sources underlying the functional damage observed by multifocal electroretinography (mfERG) responses of glaucomatous eyes of monkeys.
First- and second-order (K1 and K2, respectively) mfERG responses of three normal and three experimentally induced glaucomatous eyes of cynomolgus monkeys were measured at two different levels of luminance. Retinal contributors to the responses were isolated by intravitreal injections of pharmacological agents that suppress specific retinal cells. gamma-Aminobutyric acid (GABA) and glycine were administered to block inner retinal function, followed by 2-amino-4-phosphonobutyric acid (APB), to block ON-bipolar cells.
An inner retinal component removed by GABA and glycine was found in both the normal and glaucomatous eyes. However, it was attenuated in the latter, correlating with changes observed in the baseline K1 responses. Delays in the latency of outer retinal components were found in the responses of the glaucomatous eyes. K2 responses were dominated by an inner retinal contribution and were diminished in the responses of glaucomatous eyes. The outer retina responded to increased luminance with a shorter implicit time. A distinct wave part of the inner retinal component responded to increased luminance with increased amplitudes.
The integration of the retinal sources forming the mfERG response was compared between normal and glaucomatous monkey eyes. Both inner and outer retinal functions were aberrant in the responses of the glaucomatous eyes, with the attenuation of the inner retinal function more conspicuous. Nevertheless, glaucomatous eyes retained certain inner retinal activity, despite the advanced stage of disease. K2 responses were more sensitive to glaucomatous changes than were K1 responses.
研究猴青光眼眼中多焦视网膜电图(mfERG)反应所观察到的功能损害的细胞来源。
在两种不同亮度水平下,测量了三只正常食蟹猴和三只实验性诱导青光眼食蟹猴的一阶和二阶(分别为K1和K2)mfERG反应。通过玻璃体内注射抑制特定视网膜细胞的药物来分离对反应有贡献的视网膜成分。注射γ-氨基丁酸(GABA)和甘氨酸以阻断视网膜内层功能,随后注射2-氨基-4-磷酸丁酸(APB)以阻断ON双极细胞。
在正常眼和青光眼眼中均发现了被GABA和甘氨酸去除的视网膜内层成分。然而,在青光眼眼中该成分减弱,这与基线K1反应中观察到的变化相关。在青光眼眼的反应中发现视网膜外层成分的潜伏期延迟。K2反应主要由视网膜内层成分主导,在青光眼眼的反应中减弱。视网膜外层对亮度增加的反应潜伏期更短。视网膜内层成分的一个明显波部分对亮度增加的反应幅度增大。
比较了正常猴眼和青光眼猴眼中形成mfERG反应的视网膜来源的整合情况。在青光眼眼的反应中,视网膜内层和外层功能均异常,其中视网膜内层功能的减弱更为明显。尽管疾病已处于晚期,但青光眼眼仍保留了一定的视网膜内层活性。K2反应比K1反应对青光眼变化更敏感。