Multiple Roles for Nogo Receptor 1 in Visual System Plasticity.

Multiple Roles for Nogo Receptor 1 in Visual System Plasticity.
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DOI:
10.1177/1073858415614564
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发表时间:
2016-12
期刊:
The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
影响因子:
--
通讯作者:
McGee AW
McGee AW
中科院分区:
其他
文献类型:
--
作者:
Stephany CÉ;Frantz MG;McGee AW

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在视觉可塑性发育的关键期,不协调视觉改变了视皮层神经元的反应性。关键期的随后关闭不仅巩固了神经功能,而且限制了从先前异常视觉体验中恢复敏锐度。尽管视觉系统的电路存在物种特异性差异,但这些特征是保守的。nogo-66受体1(ngr 1)是迄今为止发现的少数对关闭关键期至关重要的基因之一。缺乏功能性ngr 1基因的小鼠在成年后仍保持发育性视觉可塑性,并且在长时间视觉剥夺后,它们的视敏度自发地提高。使用条件小鼠遗传学的实验表明,ngr 1限制了眼优势和视敏度的不同回路的可塑性。然而,NgR 1限制可塑性的机制尚未阐明,部分原因是该蛋白的亚细胞定位和信号转导仅部分了解。在这里,我们探讨了NgR 1功能的潜在机制,与重新激活成人视觉可塑性的操作有关,并提出了调查路线,以解决相关的知识空白。
During the developmental critical period for visual plasticity, discordant vision alters the responsiveness of neurons in visual cortex. The subsequent closure of the critical period not only consolidates neural function but also limits recovery of acuity from preceding abnormal visual experience. Despite species-specific differences in circuitry of the visual system, these characteristics are conserved. The nogo-66 receptor 1 (ngr1) is one of only a small number of genes identified thus far that is essential to closing the critical period. Mice lacking a functional ngr1 gene retain developmental visual plasticity as adults and their visual acuity spontaneously improves after prolonged visual deprivation. Experiments employing conditional mouse genetics have revealed that ngr1 restricts plasticity within distinct circuits for ocular dominance and visual acuity. However, the mechanisms by which NgR1 limits plasticity have not been elucidated, in part because the subcellular localization and signal transduction of the protein are only partially understood. Here we explore potential mechanisms for NgR1 function in relation to manipulations that reactivate visual plasticity in adults and propose lines of investigation to address relevant gaps in knowledge.
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