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在关键期晚期或超过关键期后沉浸于黑暗中时对单眼剥夺的易感性。

Susceptibility to monocular deprivation following immersion in darkness either late into or beyond the critical period.

作者信息

Duffy Kevin R, Lingley Alexander J, Holman Kaitlyn D, Mitchell Donald E

机构信息

Department of Psychology and Neuroscience, Dalhousie University Life Sciences Centre, Halifax, Nova Scotia, Canada, B3H 4R2.

出版信息

J Comp Neurol. 2016 Sep 1;524(13):2643-53. doi: 10.1002/cne.23985. Epub 2016 Mar 6.

DOI:10.1002/cne.23985
PMID:26878686
Abstract

An extended duration of darkness starting near the time of birth preserves immature neuronal characteristics and prolongs the accentuated plasticity observed in young animals. Brief periods of complete darkness have emerged as an effective means of restoring a high capacity for neural plasticity and of promoting recovery from the effects of monocular deprivation (MD). We examined whether 10 days of darkness imposed in adulthood or beyond the peak of the critical period could rejuvenate the ability of MD to reduce the size of neuron somata within deprived layers of the cat dorsal lateral geniculate nucleus (dLGN). For adult cats subjected to 10 days of darkness before 7 days of MD, we observed no alteration in neuron size or neurofilament labeling within the dLGN. At 12 weeks of age, MD that followed immediately after 10 days of darkness produced an enhanced reduction of neuron soma size within deprived dLGN layers. For this age we observed that 10 days of darkness also enhanced the loss of neurofilament protein within deprived dLGN layers. These results indicate that, although 10 days of darkness in adulthood does not enhance the susceptibility to 7 days of MD, darkness imposed near the trailing edge of the critical period can restore a heightened susceptibility to MD more typical of an earlier developmental stage. The loss of neurofilament in juveniles exposed to darkness prior to MD suggests that the enhanced capacity for structural plasticity is partially rooted in the ability of darkness to modulate molecules that inhibit plasticity. J. Comp. Neurol. 524:2643-2653, 2016. © 2016 Wiley Periodicals, Inc.

摘要

在出生前后开始的一段较长时间的黑暗期可保留未成熟神经元的特征,并延长在幼小动物中观察到的增强的可塑性。短暂的完全黑暗期已成为恢复神经可塑性高能力以及促进从单眼剥夺(MD)影响中恢复的有效手段。我们研究了成年期或关键期高峰期之后施加10天黑暗是否能恢复MD减少猫背外侧膝状核(dLGN)剥夺层内神经元胞体大小的能力。对于在MD 7天之前接受10天黑暗处理的成年猫,我们观察到dLGN内神经元大小或神经丝标记没有改变。在12周龄时,在10天黑暗处理后立即进行的MD导致剥夺的dLGN层内神经元胞体大小进一步减小。对于这个年龄,我们观察到10天黑暗处理也增强了剥夺的dLGN层内神经丝蛋白的丢失。这些结果表明,虽然成年期10天的黑暗不会增强对7天MD的易感性,但在关键期后期施加黑暗可以恢复更典型的早期发育阶段对MD的更高易感性。在MD之前暴露于黑暗的幼小动物中神经丝的丢失表明,增强的结构可塑性能力部分源于黑暗调节抑制可塑性分子的能力。《比较神经学杂志》524:2643 - 2653,2016年。©2016威利期刊公司。

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