Acar Katerina, Kiorpes Lynne, Movshon J Anthony, Smith Matthew A
Center for the Neural Basis of Cognition, Pittsburgh, Pennsylvania.
Center for Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania.
J Neurophysiol. 2019 Dec 1;122(6):2243-2258. doi: 10.1152/jn.00232.2019. Epub 2019 Sep 25.
Amblyopia, a disorder in which vision through one of the eyes is degraded, arises because of defective processing of information by the visual system. Amblyopia often develops in humans after early misalignment of the eyes (strabismus) and can be simulated in macaque monkeys by artificially inducing strabismus. In such amblyopic animals, single-unit responses in primary visual cortex (V1) are appreciably reduced when evoked by the amblyopic eye compared with the other (fellow) eye. However, this degradation in single V1 neuron responsivity is not commensurate with the marked losses in visual sensitivity and resolution measured behaviorally. Here we explored the idea that changes in patterns of coordinated activity across populations of V1 neurons may contribute to degraded visual representations in amblyopia, potentially making it more difficult to read out evoked activity to support perceptual decisions. We studied the visually evoked activity of V1 neuronal populations in three macaques () with strabismic amblyopia and in one control animal. Activity driven through the amblyopic eye was diminished, and these responses also showed more interneuronal correlation at all stimulus contrasts than responses driven through the fellow eye or responses in the control animal. A decoding analysis showed that responses driven through the amblyopic eye carried less visual information than other responses. Our results suggest that part of the reduced visual capacity of amblyopes may be due to changes in the patterns of functional interaction among neurons in V1. Previous work on the neurophysiological basis of amblyopia has largely focused on relating behavioral deficits to changes in visual processing by single neurons in visual cortex. In this study, we recorded simultaneously from populations of primary visual cortical (V1) neurons in macaques with amblyopia. We found changes in the strength and pattern of shared response variability between neurons. These changes in neuronal interactions could impair the visual representations of V1 populations driven by the amblyopic eye.
弱视是一种其中一只眼睛的视力下降的病症，它是由于视觉系统对信息的处理缺陷而产生的。弱视在人类中通常在眼睛早期出现错位（斜视）后发生，并且可以通过人工诱导斜视在猕猴中模拟。在这种弱视动物中，与另一只（健侧）眼睛相比，弱视眼诱发的初级视觉皮层（V1）中的单神经元反应明显减少。然而，单个V1神经元反应性的这种下降与行为测量的视觉敏感性和分辨率的显著损失并不相称。在这里，我们探讨了这样一种观点，即V1神经元群体中协调活动模式的变化可能导致弱视中视觉表征的退化，这可能使得读出诱发活动以支持感知决策变得更加困难。我们研究了三只患有斜视性弱视的猕猴和一只对照动物的V1神经元群体的视觉诱发活动。通过弱视眼驱动的活动减少，并且在所有刺激对比度下，这些反应也比通过健侧眼睛驱动的反应或对照动物中的反应表现出更多的神经元间相关性。解码分析表明，通过弱视眼驱动的反应比其他反应携带的视觉信息更少。我们的结果表明，弱视患者视觉能力下降的部分原因可能是V1中神经元之间功能相互作用模式的变化。先前关于弱视神经生理学基础的工作主要集中在将行为缺陷与视觉皮层中单个神经元的视觉处理变化联系起来。在这项研究中，我们同时记录了患有弱视的猕猴的初级视觉皮层（V1）神经元群体。我们发现神经元之间共享反应变异性的强度和模式发生了变化。这些神经元相互作用的变化可能会损害由弱视眼驱动的V1群体的视觉表征。
