Department of Neuroscience, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Department of Developmental Physiology, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
J Neurosci. 2021 Feb 24;41(8):1755-1768. doi: 10.1523/JNEUROSCI.2293-20.2020. Epub 2020 Dec 18.
After damage to the primary visual cortex (V1), conscious vision is impaired. However, some patients can respond to visual stimuli presented in their lesion-affected visual field using residual visual pathways bypassing V1. This phenomenon is called "blindsight." Many studies have tried to identify the brain regions responsible for blindsight, and the pulvinar and/or lateral geniculate nucleus (LGN) are suggested to play key roles as the thalamic relay of visual signals. However, there are critical problems regarding these preceding studies in that subjects with different sized lesions and periods of time after lesioning were investigated; furthermore, the ability of blindsight was assessed with different measures. In this study, we used double dissociation to clarify the roles of the pulvinar and LGN by pharmacological inactivation of each region and investigated the effects in a simple task with visually guided saccades (VGSs) using monkeys with a unilateral V1 lesion, by which nearly all of the contralesional visual field was affected. Inactivating either the ipsilesional pulvinar or LGN impaired VGS toward a visual stimulus in the affected field. In contrast, inactivation of the contralesional pulvinar had no clear effect, but inactivation of the contralesional LGN impaired VGS to the intact visual field. These results suggest that the pulvinar and LGN play key roles in performing the simple VGS task after V1 lesioning, and that the visuomotor functions of blindsight monkeys were supported by plastic changes in the visual pathway involving the pulvinar, which emerged after V1 lesioning. Many studies have been devoted to understanding the mechanism of mysterious symptom called "blindsight," in which patients with damage to the primary visual cortex (V1) can respond to visual stimuli despite loss of visual awareness. However, there is still a debate on the thalamic relay of visual signals. In this study, to pin down the issue, we tried double dissociation in the same subjects (hemi-blindsight macaque monkeys) and clarified that the lateral geniculate nucleus (LGN) plays a major role in simple visually guided saccades in the intact state, while both pulvinar and LGN critically contribute after the V1 lesioning, suggesting that plasticity in the visual pathway involving the pulvinar underlies the blindsight.
初级视皮层（V1）损伤后，意识性视觉会受损。然而，一些患者可以通过绕过 V1 的残余视觉通路对损伤视野中的视觉刺激做出反应，这种现象被称为“盲视”。许多研究试图确定负责盲视的脑区，而丘脑的外侧膝状体核（LGN）和/或丘脑枕被认为是视觉信号的重要中继。然而，这些先前的研究存在一些关键问题，即研究对象的损伤大小和损伤后时间不同；此外，盲视能力的评估采用了不同的测量方法。在这项研究中，我们使用药理学失活的方法来区分丘脑枕和外侧膝状体核的作用，并通过对单侧 V1 损伤的猴子进行简单的视觉引导扫视（VGS）任务来研究其影响，该任务中几乎所有的对侧视野都受到了影响。失活同侧丘脑枕或外侧膝状体核都会损害对损伤视野中视觉刺激的 VGS。相比之下，失活对侧丘脑枕没有明显影响，但失活对侧外侧膝状体核会损害对完整视野的 VGS。这些结果表明，在 V1 损伤后，丘脑枕和外侧膝状体核在执行简单的 VGS 任务中起着关键作用，而盲视猴子的视动功能是由 V1 损伤后涉及丘脑枕的视觉通路的可塑性变化所支持的。许多研究致力于理解一种被称为“盲视”的神秘症状的机制，即初级视皮层（V1）损伤的患者尽管失去了视觉意识，但仍能对视觉刺激做出反应。然而，对于视觉信号的丘脑中继仍存在争议。在这项研究中，为了明确这一问题，我们在同一受试者（半盲视猕猴）中进行了双重分离，并阐明了外侧膝状体核（LGN）在正常状态下对简单的视觉引导扫视起着主要作用，而在 V1 损伤后，丘脑枕和 LGN 都起着关键作用，这表明涉及丘脑枕的视觉通路的可塑性是盲视的基础。
