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视网膜和胼胝体活动依赖性叉头框蛋白 M1 细胞消除塑造初级视皮层的双眼视。

Retinal and Callosal Activity-Dependent Chandelier Cell Elimination Shapes Binocularity in Primary Visual Cortex.

机构信息

Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.

Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA; Interdepartmental Neuroscience Program, Yale University, New Haven, CT, USA.

出版信息

Neuron. 2021 Feb 3;109(3):502-515.e7. doi: 10.1016/j.neuron.2020.11.004. Epub 2020 Dec 7.

Abstract

In mammals with binocular vision, integration of the left and right visual scene relies on information in the center visual field, which are relayed from each retina in parallel and merge in the primary visual cortex (V1) through the convergence of ipsi- and contralateral geniculocortical inputs as well as transcallosal projections between two visual cortices. The developmental assembly of this binocular circuit, especially the transcallosal pathway, remains incompletely understood. Using genetic methods in mice, we found that several days before eye-opening, retinal and callosal activities drive massive apoptosis of GABAergic chandelier cells (ChCs) in the binocular region of V1. Blockade of ChC elimination resulted in a contralateral eye-dominated V1 and deficient binocular vision. As pre-vision retinal activities convey the left-right organization of the visual field, their regulation of ChC density through the transcallosal pathway may prime a nascent binocular territory for subsequent experience-driven tuning during the post-vision critical period.

摘要

在具有双眼视觉的哺乳动物中,左右视觉场景的整合依赖于中央视野的信息,这些信息从每个视网膜平行传递,并在初级视觉皮层 (V1) 中通过同侧和对侧外膝体-皮质输入的会聚以及两个视皮层之间的胼胝体投射融合。这个双眼回路的发育组装,特别是胼胝体通路,仍然不完全清楚。我们在小鼠中使用遗传方法发现,在睁眼前几天,视网膜和胼胝体活动会导致 V1 双眼区域 GABA 能 Chandelier 细胞 (ChC) 的大量凋亡。ChC 消除的阻断导致 V1 对侧眼优势和双眼视觉缺陷。由于预先的视觉视网膜活动传达了视野的左右组织,它们通过胼胝体通路调节 ChC 密度可能会为随后的后视觉关键期经验驱动的调谐提供一个新生的双眼区域。

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