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首页> 外文期刊>The European Journal of Neuroscience >Contribution of the retino-tectal pathway to visually guided saccades after lesion of the primary visual cortex in monkeys.
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Contribution of the retino-tectal pathway to visually guided saccades after lesion of the primary visual cortex in monkeys.

机译：猴子的主要视觉皮层病变后，视网膜-顶盖通路对视觉引导的扫视的贡献。

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Previous reports on 'blindsight' have shown that some patients with lesions of the primary visual cortex (V1) could localize visual targets in their scotoma with hand and/or eye movements without visual awareness. A role of the retino-tectal pathway on residual vision has been proposed but the direct evidence for this still remains sparse. To examine this possibility, we inactivated the superior colliculus (SC) of unilateral V1-lesioned monkeys using microinjections of muscimol, and analysed the effects on visually guided saccades. Following muscimol injections into the contralesional SC, the monkeys performed the visually guided saccade task with relatively minor deficits. The effects of ipsilesional SC inactivation were more severe. After injections, the monkeys failed to localize the target within the visual field represented at the injection site on the SC map. The effects of ipsilesional SC inactivation may result from sensory deficits, motor deficits or a combination of both. To examine these possibilities, we tested the effects of SC inactivation on the motor system by investigating spontaneous saccades. After inactivation of the ipsilesional SC, spontaneous saccades toward the injection site were not abolished, suggesting that impairment of visually guided saccades following inactivation of the ipsilesional SC could not be explained solely by a motor deficit and was primarily due to a visual deficit, presumably by interfering with processing in the superficial layer. We conclude that the retino-tectal pathway plays an essential role in residual vision after V1 lesion. The results suggest that this pathway may be involved in mediating unconscious vision in blindsight patients.
机译：先前有关“视力不佳”的报告表明，一些患有原发性视皮层（V1）病变的患者可以通过手和/或眼球运动将其视觉定位在他们的暗室中，而没有视觉意识。视网膜-视网膜通路对残余视力的作用已被提出，但是其直接证据仍然很少。为了检验这种可能性，我们使用微量注射麝香酚灭活了单侧V1病变猴子的上丘（SC），并分析了对视觉引导扫视的影响。在向对侧SC中注射麝香酚之后，猴子以视觉引导的扫视任务进行了相对较小的缺陷。同病SC失活的影响更为严重。注射后，猴子无法将目标定位在SC图上注射部位所代表的视野内。同病SC失活的影响可能是由于感觉缺陷，运动缺陷或两者的结合。为了检查这些可能性，我们通过研究自发扫视测试了SC失活对电机系统的影响。灭活SC后，自发性扫视并没有消失，这提示灭活SC后视觉引导的扫视障碍不能仅由运动障碍来解释，而主要是由于视力缺陷，大概是由于干扰表层的处理。我们得出的结论是，视网膜-枕叶通路在V1病变后的残余视力中起着至关重要的作用。结果表明，该途径可能参与调节视力不佳患者的潜意识。

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