Viswanathan S, Frishman L J, Robson J G, Harwerth R S, Smith E L
College of Optometry, University of Houston, Texas 77204-6052, USA.
Invest Ophthalmol Vis Sci. 1999 May;40(6):1124-36.
To investigate the photopic flash electroretinograms (ERGs) of macaque monkeys in which visual field defects developed as a consequence of experimental glaucoma.
Unilateral experimental glaucoma was induced in 10 monkeys by argon laser treatment of the trabecular meshwork. Visual field sensitivity was assessed behaviorally by static perimetry. Photopic ERGs were recorded to brief- (< or = 5 msec) and long-duration (200 msec) red ganzfeld flashes on a rod-suppressing blue-adapting background. Electroretinograms were recorded in four other monkeys, after intravitreal injection of tetrodotoxin (TTX; 3.8-8 p.M) to suppress action potentials of retinal ganglion and amacrine cells, and in six normal adult human subjects.
Experimental glaucoma removed a cornea-negative response, the photopic-negative response (PhNR), from the ERG. The PhNR in control eyes was maximal approximately 60 msec after a brief flash, 100 msec after onset, and 115 msec after offset of the long-duration stimulus. The PhNR in experimental eyes was greatly reduced when the mean deviation of the visual field sensitivity was as little as -6 dB. As visual sensitivity declined further, the PhNR was reduced only slightly more. The a- and b-waves were unchanged, even when sensitivity decreased by more than 16 dB. Tetrodotoxin also selectively reduced the PhNR. The PhNR was observed in normal human ERGs.
The cornea-negative PhNR of the photopic ERG depends on spiking activity and is reduced in experimental glaucoma when visual sensitivity losses are still mild. The PhNR most likely arises from retinal ganglion cells and their axons, but its slow timing raises the possibility that it could be mediated by glia. Regardless of the mechanism of its generation, the PhNR holds promise as an indicator of retinal function in early glaucomatous optic neuropathy.
研究因实验性青光眼导致视野缺损的猕猴的明视闪光视网膜电图（ERG）。
通过氩激光小梁网治疗诱导10只猴子发生单侧实验性青光眼。通过静态视野计行为评估视野敏感性。在抑制视杆细胞的蓝色适应背景下，记录对短（≤5毫秒）和长持续时间（200毫秒）红色全视野闪光的明视ERG。在另外4只猴子玻璃体内注射河豚毒素（TTX；3.8 - 8 p.M）以抑制视网膜神经节细胞和无长突细胞的动作电位后记录视网膜电图，并在6名正常成年人中进行记录。
实验性青光眼使ERG中的角膜负反应，即明视负反应（PhNR）消失。对照眼的PhNR在短闪光后约60毫秒、长持续时间刺激开始后100毫秒和结束后115毫秒时最大。当视野敏感性平均偏差低至 -6 dB时，实验眼的PhNR大幅降低。随着视觉敏感性进一步下降，PhNR仅略有降低。a波和b波未改变，即使敏感性下降超过16 dB。河豚毒素也选择性地降低了PhNR。在正常人ERG中观察到了PhNR。
明视ERG的角膜负PhNR依赖于锋电位活动，并且在实验性青光眼中当视觉敏感性损失仍较轻微时降低。PhNR最可能起源于视网膜神经节细胞及其轴突，但其缓慢的时间进程增加了它可能由神经胶质细胞介导的可能性。无论其产生机制如何，PhNR有望作为早期青光眼性视神经病变中视网膜功能的指标。
