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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1
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Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1

机译：通过揭露Lynx1揭露成人视皮层可塑性的蛋白水解活性。

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摘要

Experience-dependent cortical plasticity declines with age. At the molecular level, experience-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in the adult brain if mice are raised in standard cages. Understanding the mechanism for the loss of permissive proteolytic activity is therefore a key link for improving function in adult brains. Using the mouse primary visual cortex (V1) as a model, we demonstrate that tPA activity in V1 can be unmasked following 4 d of monocular deprivation when the mice older than 2 months are raised in standard cages by the genetic removal of Lynx1, a negative regulator of adult plasticity. This was also associated with the reduction of stubby and thin spine density and enhancement of ocular dominance shift in adult V1 of Lynx1 knock-out ( KO) mice. These structural and functional changes were tPA-dependent because genetic removal of tPA in Lynx1 KO mice can block the monocular deprivation-dependent reduction of dendritic spine density, whereas both genetic and adult specific inhibition of tPA activity can ablate the ocular dominance shift in Lynx1 KO mice. Our work demonstrates that the adult brain has an intrinsic potential for experience-dependent elevation of proteolytic activity to express juvenile-like structural and functional changes but is effectively limited by Lynx1 if mice are raised in standard cages. Insights into the Lynx1-tPA plasticity mechanism may provide novel therapeutic targets for adult brain disorders.
机译：经验依赖的皮质可塑性随着年龄的增长而下降。在分子水平上，如果将小鼠放在标准笼中饲养，成年脑组织纤溶酶原激活物（tPA）的经验依赖性蛋白水解活性将受到限制。因此，了解丧失允许的蛋白水解活性的机制是改善成年大脑功能的关键环节。使用小鼠初级视觉皮层（V1）作为模型，我们证明了当通过基因去除Lynx1在阴性笼中饲养大于2个月的小鼠时，在单眼剥夺4 d后可以揭露V1中的tPA活性，成人可塑性的调节剂。这还与降低Lynx1基因敲除（KO）小鼠的成年V1的粗短和较薄的脊柱密度和增强眼部优势有关。这些结构和功能变化是tPA依赖性的，因为在Lynx1 KO小鼠中tPA的遗传去除可以阻止单眼剥夺依赖性的树突棘密度降低，而对tPA活性的遗传抑制和成年特异性抑制都可以消除Lynx1 KO的眼球优势转移老鼠。我们的工作表明，成年大脑具有依赖经验的蛋白水解活性来表达类似青少年的结构和功能变化的内在潜力，但是如果在标准笼中饲养小鼠，Lynx1可以有效地限制它。对Lynx1-tPA可塑性机制的见解可能为成人脑部疾病提供新的治疗靶标。

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