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早期单眼视网膜损伤后猫17区的地形图重组

Topographic map reorganization in cat area 17 after early monocular retinal lesions.

作者信息

Matsuura Kazuki, Zhang Bin, Mori Takafumi, Smith Earl L, Kaas Jon H, Chino Yuzo

机构信息

College of Optometry, University of Houston, TX 77204-2020, USA.

出版信息

Vis Neurosci. 2002 Jan-Feb;19(1):85-96. doi: 10.1017/s095252380119108x.

Abstract

Neither discrete peripheral retinal lesions nor the normal optic disk produces obvious holes in one's percept of the world because the visual brain appears to perceptually "fill in" these blind spots. Where in the visual brain or how this filling in occurs is not well understood. A prevailing hypothesis states that topographic map of visual cortex reorganizes after retinal lesions, which "sews up" the hole in the topographic map representing the deprived area of cortex (cortical scotoma) and may lead to perceptual filling in. Since the map reorganization does not typically occur unless retinotopically matched lesions are made in both eyes, we investigated the conditions in which monocular retinal lesions can induce comparable map reorganization. We found that following monocular retinal lesions, deprived neurons in cat area 17 can acquire new receptive fields if the lesion occurred relatively early in life (8 weeks of age) and the lesioned cats experienced a substantial period of recovery (>3 years). Quantitative determination of the monocular and binocular response properties of reactivated units indicated that responses to the lesioned eye for such neurons were remarkably robust, and that the receptive-field properties for the two eyes were generally similar. Moreover, excitatory or inhibitory binocular interactions were found in the majority of experimental units when the two eyes were activated together. These results are consistent with the hypothesis that map reorganization after monocular retinal lesions require experience-dependent plasticity and may be involved in the perceptual filling in of blind spots due to retinal lesions early in life.

摘要

离散的周边视网膜病变和正常的视盘都不会在人的世界感知中产生明显的空洞,因为视觉脑似乎在感知上“填补”了这些盲点。视觉脑中的这个填补过程发生在哪里以及如何发生,目前还不太清楚。一个普遍的假说是,视网膜病变后视觉皮层的地形图会重新组织,这“缝合”了代表皮层剥夺区域(皮层暗点)的地形图中的空洞,并可能导致感知填补。由于除非双眼进行视网膜拓扑匹配的损伤,否则这种地形图重组通常不会发生,我们研究了单眼视网膜损伤可诱导类似地形图重组的条件。我们发现,单眼视网膜损伤后,如果损伤发生在相对较早的生命阶段(8周龄),且损伤的猫经历了较长的恢复时间(>3年),猫17区的被剥夺神经元可以获得新的感受野。对重新激活单元的单眼和双眼反应特性的定量测定表明,此类神经元对损伤眼的反应非常强烈,且两只眼睛的感受野特性通常相似。此外,当两只眼睛同时被激活时,在大多数实验单元中发现了兴奋性或抑制性的双眼相互作用。这些结果与以下假说一致:单眼视网膜损伤后的地形图重组需要经验依赖性可塑性,并且可能参与了生命早期因视网膜损伤导致的盲点的感知填补。

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