Grüsser O J, Grüsser-Cornehls U, Hagner M, Przybyszewski A W
Department of Physiology, Freie Universität, Berlin, Germany.
Physiol Bohemoslov. 1989;38(4):289-309.
(a) When a subject indents one of his eyeballs in total darkness, he immediately perceives light extending slowly across the whole visual field of the indented eye. The appearance and the time course of these pressure or deformation phosphenes are described. (b) With simultaneous binocular indentation of the eyeballs a flickering patterned phosphene is observed. (c) A short history of the research on pressure phosphenes and its consequences for the theories of vision is presented. (d) Purkynĕ's observations of monocular deformation phosphenes are described. He repeatedly noted patterned light structures, which most observers only perceive with simultaneous binocular eyeball deformation. It is suggested that Purkynĕ's deviating observations were caused by amblyopia of one eye. (e) The neurophysiological basis of the monocular pressure phosphenes was investigated by means of microelectrode recordings from single optic tract fibers. The activity of single retinal ganglion cells (on-center, off-center neurons, latency class I [Y-neurons] or latency class II [X-neurons]), was recorded in anaesthetized cats. Eyeball deformation in total darkness led to an activation of the on-center ganglion cells, while the off-center ganglion cells were inhibited. The latency and strength of this activation or inhibition varied considerably between different neurons, but were fairly constant in the same neuron when the eyeball indentation was repeated after a pause of 1-3 min. The latency and strength of neuronal activation or inhibition seemed to be dependent mainly upon the neuron location relative to the point of eyeball indentation. Some on-center neurons also exhibited a short activation at "deformation off". (f) The antagonistic response type of on-center and off-center ganglion cells was also observed when the eyeball was deformed as a hydrostatic open system and the intraocular pressure was kept at 25 mm Hg basic pressure. (g) Dark adaptation up to 45 min affected the deformation responses of retinal neurons only to a small degree, if at all. This corresponds to the observation that deformation phosphenes in a human observer changed little during the course of dark adaptation. (h) We assume that the activation of on-center and inhibition of off-center ganglion cells by eyeball deformation are caused by retinal stretching, which also leads to horizontal cell stretch. Stretching the horizontal cell membrane probably generates an increase in membrane sodium conductivity and a depolarization of the membrane potential. This depolarization of the horizontal cell membrane potential is transmitted either directly or indirectly (via receptor synapses) from the horizontal to the bipolar cells.(ABSTRACT TRUNCATED AT 400 WORDS)
(a) 当受试者在完全黑暗中压陷其一只眼球时,他会立即感觉到有光线缓慢地在被压陷眼球的整个视野中蔓延。文中描述了这些压力性或变形性光幻视的外观及时间过程。(b) 双眼同时压陷眼球时,会观察到一种闪烁的图案状光幻视。(c) 介绍了压力性光幻视的研究简史及其对视觉理论的影响。(d) 描述了浦肯野对单眼变形性光幻视的观察。他多次注意到图案状的光结构,而大多数观察者只有在双眼同时眼球变形时才会察觉到。有人认为浦肯野的异常观察是由一只眼睛的弱视引起的。(e) 通过对单根视束纤维进行微电极记录,研究了单眼压陷性光幻视的神经生理基础。在麻醉的猫身上记录单个视网膜神经节细胞(中心兴奋型、中心抑制型神经元,潜伏期I类 [Y神经元] 或潜伏期II类 [X神经元])的活动。在完全黑暗中眼球变形会导致中心兴奋型神经节细胞激活,而中心抑制型神经节细胞受到抑制。这种激活或抑制的潜伏期和强度在不同神经元之间有很大差异,但当眼球压陷在停顿1 - 3分钟后重复时,同一神经元中的情况相当稳定。神经元激活或抑制的潜伏期和强度似乎主要取决于神经元相对于眼球压陷点的位置。一些中心兴奋型神经元在“变形停止”时也会出现短暂激活。(f) 当眼球作为一个流体静力开放系统变形且眼内压保持在25 mmHg基础压力时,也观察到了中心兴奋型和中心抑制型神经节细胞的拮抗反应类型。(g) 长达45分钟的暗适应对视网膜神经元的变形反应影响甚微,即便有影响也很小。这与人类观察者在暗适应过程中变形性光幻视变化不大的观察结果相符。(h) 我们假设眼球变形对中心兴奋型神经节细胞激活及中心抑制型神经节细胞抑制是由视网膜拉伸引起的,这也会导致水平细胞拉伸。拉伸水平细胞膜可能会使膜钠电导率增加,膜电位去极化。水平细胞膜电位的这种去极化会直接或间接地(通过受体突触)从水平细胞传递到双极细胞。(摘要截选至400字)