Enhancement of visual cortex plasticity by dark exposure.
Enhancement of visual cortex plasticity by dark exposure.
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通过黑暗暴露增强视觉皮层可塑性。
DOI：
10.1098/rstb.2016.0159
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发表时间：
2017-03-05
期刊：
影响因子：
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通讯作者：
Sengpiel F
中科院分区：
文献类型：
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作者：
Erchova I;Vasalauskaite A;Longo V;Sengpiel F
已知暗饲养延迟视皮层中眼优势可塑性的关键期的时间过程。最近的证据表明，一段时间的黑暗暴露（DE）可能会增强或恢复可塑性，即使在关闭的关键时期，通过修改的兴奋-抑制平衡和/或删除结构制动可塑性介导。在这里，我们研究了一个星期的DE对恢复从一个月的单眼剥夺（MD）在初级视觉皮层（V1）的幼年小鼠。内在信号的光学成像显示，接受DE的小鼠V1的眼优势比未接受DE的小鼠恢复得稍快，但三周后两组的恢复水平相似。双光子钙离子成像显示两组兴奋性神经元方向选择性恢复无显著差异。小清蛋白阳性（PV+）的中间神经元表现出较小的眼优势转移在MD，但再次没有差异，在随后的恢复。与没有DE的小鼠相比，有DE的小鼠中被神经束膜网（可塑性的结构制动器）包围的PV+细胞的百分比较低。总的来说，DE导致小鼠视觉皮层可塑性的适度增强。这篇文章是“整合赫布和稳态可塑性”主题问题的一部分。
Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.