Binocular Input Coincidence Mediates Critical Period Plasticity in the Mouse Primary Visual Cortex
Binocular Input Coincidence Mediates Critical Period Plasticity in the Mouse Primary Visual Cortex
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双眼输入重合介导小鼠初级视觉皮层的关键期可塑性
DOI：
10.1523/jneurosci.2640-13.2014
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发表时间：
2014-02-19
影响因子：
5.3
通讯作者：
Zhang, Xiao-hui
中科院分区：
文献类型：
--
作者：
Chen, Xiao-jing;Rasch, Malte J.;Zhang, Xiao-hui
关于初级视觉皮质(V1)眼优势(OD)组织发育的经典研究揭示了一个出生后关键期(CP)，在此期间，双眼之间的视觉输入最有效地通过突触竞争来塑造皮质回路。在CP期间，短暂闭上一只眼睛导致V1神经元的反应偏好明显向睁开的眼睛移动，这是发育中的V1的一种CP可塑性形式。然而，目前还不清楚在CP过程中双眼输入的什么特殊性质负责调节这种经验依赖的外径可塑性。在小鼠V1的全细胞记录中，我们发现在CP期间，从双眼到第2/3层和第4层双眼细胞的视觉驱动突触输入变得高度一致。通过脑内注射安定来增强皮质GABA能传递活性，不仅导致CP前期小鼠双眼输入和外径可塑性高度一致的早熟发作，而且在黑暗饲养的小鼠中拯救了这两者，表明双眼输入和CP可塑性之间存在紧密联系。在Thy1-ChR2小鼠中，在CP期间，视网膜神经节细胞的异步光遗传激活导致这种双眼输入符合的慢性破坏，取消了外径可塑性。使用前馈网络模型的计算机模拟进一步表明，重合的输入可以通过带有突触竞争的稳态突触学习机制来调节这种CP可塑性。这些结果表明，双眼输入的高水平相关性是发育中V1的CP的一个标志，并为外向可塑性的诱导提供了神经底物。
Classical studies on the development of ocular dominance (OD) organization in primary visual cortex (V1) have revealed a postnatal critical period (CP), during which visual inputs between the two eyes are most effective in shaping cortical circuits through synaptic competition. A brief closure of one eye during CP caused a pronounced shift of response preference of V1 neurons toward the open eye, a form of CP plasticity in the developing V1. However, it remains unclear what particular property of binocular inputs during CP is responsible for mediating this experience-dependent OD plasticity. Using whole-cell recording in mouse V1, we found that visually driven synaptic inputs from the two eyes to binocular cells in layers 2/3 and 4 became highly coincident during CP. Enhancing cortical GABAergic transmission activity by brain infusion with diazepam not only caused a precocious onset of the high coincidence of binocular inputs and OD plasticity in pre-CP mice, but rescued both of them in dark-reared mice, suggesting a tight link between coincident binocular inputs and CP plasticity. In Thy1-ChR2 mice, chronic disruption of this binocular input coincidence during CP by asynchronous optogenetic activation of retinal ganglion cells abolished the OD plasticity. Computational simulation using a feed-forward network model further suggests that the coincident inputs could mediate this CP plasticity through a homeostatic synaptic learning mechanism with synaptic competition. These results suggest that the high-level correlation of binocular inputs is a hallmark of the CP of developing V1 and serves as neural substrate for the induction of OD plasticity.