Eskin T A, Lapham L W, Maurissen J P, Merigan W H
Invest Ophthalmol Vis Sci. 1985 Mar;26(3):317-29.
Oral acrylamide dosing for 6-10 weeks produced axonal swellings with neurofilament accumulation in the distal optic tract and lateral geniculate nucleus of macaques. No swellings were seen in the retina or optic nerve. Monkeys that were killed 6-8 months after similar dosing showed a marked neuronal degeneration in the visual pathways that was more pronounced after two than after a single period of exposure. This degeneration was characterized by the following: loss of ganglion cells in central retina with relative sparing of other retinal neurons; disproportionate degeneration of temporal to central optic nerve and the dorsal optic tract; and neuronal atrophy in parvocellular layers of the lateral geniculate nucleus, with relative sparing of magnocellular layers. The pattern of neuronal loss suggests that one type of retinal ganglion cell or its axon may be especially vulnerable to damage by acrylamide. The selective neuronal damage produced by acrylamide may help explain the nature of the visual dysfunction associated with this intoxication.
给猕猴口服丙烯酰胺6 - 10周，会在其视束远端和外侧膝状核产生轴突肿胀并伴有神经丝积聚。视网膜或视神经中未见肿胀。在类似给药后6 - 8个月处死的猴子，其视觉通路出现明显的神经元变性，在经历两个周期而非一个周期的暴露后更为明显。这种变性具有以下特征：中央视网膜神经节细胞缺失，而其他视网膜神经元相对保留；颞侧视神经和背侧视束相对于中央视神经的不成比例变性；外侧膝状核小细胞层的神经元萎缩，大细胞层相对保留。神经元丢失的模式表明，一种视网膜神经节细胞类型或其轴突可能特别容易受到丙烯酰胺的损伤。丙烯酰胺造成的选择性神经元损伤可能有助于解释这种中毒相关视觉功能障碍的性质。
