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环境丰容部分修复了早期关键期 ten-m3 敲除小鼠皮质下映射错误。

Environmental Enrichment Partially Repairs Subcortical Mapping Errors in Ten-m3 Knock-Out Mice during an Early Critical Period.

机构信息

Discipline of Physiology, School of Medical Sciences and Bosch Institute, Faculty of Medicine and Health, University of Sydney, New South Wales 2006, Australia.

Discipline of Physiology, School of Medical Sciences and Bosch Institute, Faculty of Medicine and Health, University of Sydney, New South Wales 2006, Australia

出版信息

eNeuro. 2019 Dec 9;6(6). doi: 10.1523/ENEURO.0478-18.2019. Print 2019 Nov/Dec.

Abstract

Environmental enrichment (EE) has been shown to improve neural function via the regulation of cortical plasticity. Its capacity to induce functional and/or anatomical repair of miswired circuits is unknown. Ten-m3 knock-out (KO) mice exhibit a highly stereotyped and profound miswiring of ipsilateral retinogeniculate axons and associated deficits in binocularly-mediated visual behavior. We determined whether, and when, EE can drive the repair of subcortical wiring deficits by analyzing Ten-m3 KO and wild-type (WT) mice that were enriched for six weeks from adulthood, weaning or birth in comparison to standard-housed (SE) controls. Six weeks of EE initiated from birth, but not later, induced a significant reduction in the area occupied by ipsilateral retinogeniculate terminals in KOs. No EE-induced correction of mistargeted axons was observed at postnatal day (P)7, indicating that this intervention impacts pruning rather than initial targeting of axons. This reduction was most prominent in the ventrolateral region of the dorsal lateral geniculate nucleus (dLGN), suggesting a preferential pruning of the most profoundly mistargeted axons. EE can thus partially repair a specific, subcortical axonal wiring deficit, but only during an early, developmentally-restricted time window.

摘要

环境富集(EE)已被证明可以通过调节皮质可塑性来改善神经功能。其诱导功能和/或解剖修复错误连接的电路的能力尚不清楚。Ten-m3 敲除(KO)小鼠表现出同侧视网膜神经节细胞轴突高度刻板和深刻的错误连接,并伴有双眼介导的视觉行为缺陷。我们通过分析从成年、断奶或出生开始接受六周富集 EE 的 Ten-m3 KO 和野生型(WT)小鼠,确定 EE 是否以及何时可以驱动亚皮质布线缺陷的修复,与标准饲养(SE)对照相比。从出生开始但不是之后的六周 EE 诱导,在 KO 中显著减少了同侧视网膜神经节细胞轴突末端占据的区域。在出生后第 7 天(P)未观察到 EE 诱导的错误靶向轴突的纠正,表明这种干预影响轴突的修剪而不是初始靶向。这种减少在背外侧膝状核(dLGN)的腹外侧区域最为明显,表明最严重错误靶向的轴突优先修剪。因此,EE 可以部分修复特定的、亚皮质的轴突布线缺陷,但仅在早期、发育受限的时间窗口内。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b2c/6901682/8f40cf06e6ae/enu9991931280001.jpg

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