Wietsma J J, Kamermans M, Spekreijse H
Graduate School Neurosciences Amsterdam, Laboratory of Medical Physics and Informatics, University of Amsterdam, The Netherlands.
Vision Res. 1995 Jun;35(12):1667-74. doi: 10.1016/0042-6989(94)00213-6.
Ethambutol, a tuberculostatic drug, induces red-green colour vision defects in man and goldfish. The ethambutol-induced red-green colour vision defect in goldfish was argued to originate in the retina because after ethambutol application: (1) inhibitive interactions in red-green (double) opponent ganglion cells are lost [Van Dijk & Spekreijse, 1982 (Investigative Ophthalmology and Visual Science, 24, 128-133); Wietsma & Spekreijse, 1992 (Investigative Ophthalmology and Visual Science Suppl., 33, 1032)] and (2) the depolarizing responses to red light in the biphasic horizontal cells are reduced. To account for these findings Spekreijse, Wietsma and Neumeyer [(1991) Vision Research, 31, 551-562] suggested that ethambutol induced dark adaptation in the retina. In this paper the dark adaptation hypothesis is tested with the following results: (1) ethambutol changes only transiently the receptive field size and spectral sensitivity of horizontal cells; (2) the spectral characteristics of horizontal cells do not change in long-term ethambutol-treated goldfish; (3) formation of spinules on horizontal cell dendrites in cone terminals, a parameter for light adaptation, remains unaffected. Therefore we conclude that ethambutol does not induce functional dark adaptation of horizontal cells and that the ethambutol-induced red-green colour vision deficiency does not originate in the horizontal cell layers.
乙胺丁醇是一种抗结核药物，可导致人类和金鱼出现红绿色觉缺陷。有人认为，乙胺丁醇诱导的金鱼红绿色觉缺陷起源于视网膜，因为在应用乙胺丁醇后：(1) 红绿色（双）拮抗神经节细胞中的抑制性相互作用丧失 [Van Dijk & Spekreijse, 1982（《Investigative Ophthalmology and Visual Science》，24, 128 - 133）；Wietsma & Spekreijse, 1992（《Investigative Ophthalmology and Visual Science Suppl.》，33, 1032）]，以及 (2) 双相水平细胞对红光的去极化反应减弱。为了解释这些发现，Spekreijse、Wietsma 和 Neumeyer [（1991）《Vision Research》，31, 551 - 562] 提出乙胺丁醇诱导视网膜出现暗适应。在本文中，对暗适应假说进行了测试，结果如下：(1) 乙胺丁醇仅短暂改变水平细胞的感受野大小和光谱敏感性；(2) 在长期接受乙胺丁醇治疗的金鱼中，水平细胞的光谱特性没有变化；(3) 视锥终末水平细胞树突上的棘状小体形成，这是光适应的一个参数，不受影响。因此，我们得出结论，乙胺丁醇不会诱导水平细胞发生功能性暗适应，并且乙胺丁醇诱导的红绿色觉缺陷并非起源于水平细胞层。
