Cang Jianhua, Rentería René C, Kaneko Megumi, Liu Xiaorong, Copenhagen David R, Stryker Michael P
W. M. Keck Foundation Center for Integrative Neuroscience, Department of Physiology, University of California, San Francisco, San Francisco, California 94143, USA.
Neuron. 2005 Dec 8;48(5):797-809. doi: 10.1016/j.neuron.2005.09.015.
The visual cortex is organized into retinotopic maps that preserve an orderly representation of the visual world, achieved by topographically precise inputs from the lateral geniculate nucleus. We show here that geniculocortical mapping is imprecise when the waves of spontaneous activity in the retina during the first postnatal week are disrupted genetically. This anatomical mapping defect is present by postnatal day 8 and has functional consequences, as revealed by optical imaging and microelectrode recording in adults. Pharmacological disruption of these retinal waves during the first week phenocopies the mapping defect, confirming both the site and the timing of the disruption in neural activity responsible for the defect. Analysis shows that the geniculocortical miswiring is not a trivial or necessary consequence of the retinogeniculate defect. Our findings demonstrate that disrupting early spontaneous activity in the eye alters thalamic connections to the cortex.
视觉皮层被组织成视网膜拓扑图，这些图通过来自外侧膝状体核的地形精确输入，保留了视觉世界的有序表征。我们在此表明，当出生后第一周视网膜的自发活动波因基因干扰而受到破坏时，膝状体到皮层的映射是不精确的。这种解剖学映射缺陷在出生后第8天就已出现，并具有功能后果，这在成年动物的光学成像和微电极记录中得到了揭示。在第一周对这些视网膜波进行药理学干扰可模拟这种映射缺陷，证实了导致该缺陷的神经活动干扰的部位和时间。分析表明，膝状体到皮层的错误连接并非视网膜到膝状体缺陷的微不足道或必然结果。我们的研究结果表明，破坏眼睛早期的自发活动会改变丘脑与皮层的连接。
