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Polysialylated - neural cell adhesion molecule (PSA-NCAM) promotes recovery of vision after the critical period.
Molecular and Cellular Neuroscience ( IF 3.5 ) Pub Date : 2020-07-04 , DOI: 10.1016/j.mcn.2020.103527
Margaret Po-Shan Luke 1 , Richard E Brown 2 , David B Clarke 3
Affiliation  

Vision loss has long since been considered irreversible after a critical period; however, there is potential to restore limited vision, even in adulthood. This phenomenon is particularly pronounced following complete loss of vision in the dominant eye. Adult neural cell adhesion molecule (NCAM) knockout mice have an age-related impairment of visual acuity. The underlying cause of early deterioration in visual function remains unknown. Polysialylated (PSA) NCAM is involved in different forms of neural plasticity in the adult brain, raising the possibility that NCAM plays a role in the plasticity of the visual cortex, and therefore, in visual ability. Here, we examined whether PSA-NCAM is required for visual cortical plasticity in adult C57Bl/6J mice following deafferentation and long-term monocular deprivation. Our results show that elevated PSA in the contralateral visual cortex of the reopened eye is accompanied by changes in other markers of neural plasticity: increased brain-derived neurotrophic factor (BDNF) levels and degradation of perineuronal nets (PNNs). The removal of PSA-NCAM in the visual cortex of these mice reduced BDNF expression, decreased PNN degradation, and resulted in impaired recovery of visual acuity after optic nerve transection and chronic monocular deprivation. Collectively, our results demonstrate that PSA-NCAM is necessary for the reactivation of visual cortical plasticity and recovery of visual function in adult mice. It also offers a potential molecular target for the therapeutic treatment of cortically based visual impairments.



中文翻译:

Polysialylated - 神经细胞粘附分子 (PSA-NCAM) 促进关键期后视力的恢复。

长期以来,视力丧失一直被认为是在关键时期后不可逆转的;然而,即使在成年期,也有可能恢复有限的视力。这种现象在优势眼完全丧失视力后尤为明显。成年神经细胞粘附分子 (NCAM) 敲除小鼠具有与年龄相关的视力损伤。视觉功能早期恶化的根本原因仍然未知。聚唾液酸化 (PSA) NCAM 参与成人大脑中不同形式的神经可塑性,这提高了 NCAM 在视觉皮层的可塑性中发挥作用的可能性,因此,在视觉能力中。在这里,我们检查了成人 C57Bl/6J 小鼠在传入神经传入和长期单眼剥夺后的视觉皮层可塑性是否需要 PSA-NCAM。我们的结果表明,重新打开的眼睛对侧视觉皮层中 PSA 的升高伴随着其他神经可塑性标志物的变化:脑源性神经营养因子 (BDNF) 水平增加和神经周围网络 (PNN) 退化。在这些小鼠的视觉皮层中去除 PSA-NCAM 降低了 BDNF 表达,减少了 PNN 降解,并导致视神经横断和慢性单眼剥夺后视力恢复受损。总的来说,我们的结果表明 PSA-NCAM 对于成年小鼠视觉皮层可塑性的重新激活和视觉功能的恢复是必要的。它还为基于皮质的视觉障碍的治疗提供了潜在的分子靶点。

更新日期:2020-07-16
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