Singer W, von Grünau M, Rauschecker J
Exp Brain Res. 1980;40(3):294-304. doi: 10.1007/BF00237794.
In two cats in which surgically induced, unilateral divergent strabismus had led to behaviourally determined amblyopia, a variety of electrophysiological parameters were determined in search of neuronal correlates of squint amblyopia. Tests that assess global neuronal excitability along the pathways from the two eyes to the visual cortex (areas 17 and 18) failed to reflect the functional inferiority of the squinting eye: retinographic responses and cortical evoked potentials elicited by Ganzfeld-stimulation and by stimulation of the optic nerves were identical for the two eyes. The ocular dominance distribution of neurons in area 17 showed the expected disruption of binocularity but failed to provide clear evidence for a functional inferiority of the squinting eye. At other levels of analysis, however, a clear difference between the two eyes was apparent: 1. Responses to optimally aligned light stimuli tended to be more sluggish and the under-representation of neurons with vertically oriented receptive fields was more pronounced in neurons driven from the deviated eye than in cells dominated by the normal one. 2. Interocular inhibition as assessed from electrically evoked potentials was found to be asymmetric; responses evoked from the amblyopic eye were suppressed more readily and over longer periods by conditioning shocks applied to the normal nerve than vice versa. 3. Numerous abnormalities reflecting the functional inferiority of the squinting eye became apparent in cortical potentials evoked by phase reversal of gratings of variable spatial frequency and contrast. A laminar analysis of these field potentials suggests impaired transmission along the intracortical pathways which relay activity to supragranular layers as a major cause for abnormal responses from the squinting eye. It is concluded that squint amblyopia is associated with a variety of neuronal changes at various levels of the visual levels of the visual system, the present data providing evidence for alterations at the cortical level.
在两只因手术诱发单侧散开性斜视而导致行为学确定的弱视猫中,测定了多种电生理参数,以寻找斜视性弱视的神经元相关因素。评估从双眼到视觉皮层(17区和18区)的通路中整体神经元兴奋性的测试未能反映斜视眼的功能劣势:双眼的视网膜电图反应以及全视野刺激和视神经刺激所诱发的皮层诱发电位是相同的。17区神经元的眼优势分布显示出预期的双眼性破坏,但未能为斜视眼的功能劣势提供明确证据。然而,在其他分析层面,两只眼睛之间存在明显差异:1. 对最佳对齐光刺激的反应往往更迟缓,并且与正常眼主导的细胞相比,由斜视眼驱动的神经元中垂直取向感受野神经元的代表性不足更为明显。2. 从电诱发电位评估的眼间抑制是不对称的;通过对正常神经施加条件性电击,弱视眼诱发的反应比相反情况更容易且在更长时间内受到抑制。3. 在由可变空间频率和对比度的光栅相位反转诱发的皮层电位中,许多反映斜视眼功能劣势的异常变得明显。对这些场电位的层流分析表明,沿着将活动传递到颗粒上层的皮层内通路的传递受损是斜视眼异常反应的主要原因。结论是,斜视性弱视与视觉系统各级视觉水平的多种神经元变化有关,目前的数据为皮层水平的改变提供了证据。