p75NTR作为分子记忆开关

Shen Ning, Mehdi Jorfi
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引用次数: 0

摘要

近年来,人们对许多分子和环境因素进行了研究,以了解突触可塑性是如何调节的。睡眠作为一种进化保守的生物功能,已被证明是巩固和过滤记忆痕迹下突触电路的关键角色。尽管睡眠障碍不会改变正常的记忆巩固,但它们可能反映出基本的神经回路故障,而这种故障可能在加剧自闭症和阿尔茨海默病等疾病中发挥重要作用。最近,科学家们试图回答这个谜题的一部分,他们发现p75神经营养受体(p75NTR)在调节睡眠剥夺时海马依赖性联想可塑性的损伤中起着关键作用。本文将回顾p75NTR的作用,批判性地讨论该研究作为睡眠研究和神经系统疾病的桥梁的影响和意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
p75NTR as a Molecular Memory Switch
In recent years, many molecular and environmental factors have been studied to understand how synaptic plasticity is modulated. Sleep, as an evolutionary conserved biological function, has shown to be a critical player for the consolidation and filtering of synaptic circuitry underlying memory traces. Although sleep disturbances do not alter normal memory consolidation, they may reflect fundamental circuit malfunctions that can play a significant role in exacerbating diseases, such as autism and Alzheimer’s disease. Very recently, scientists sought to answer part of this enigma and they identified p75 neurotrophic receptor (p75NTR) as a critical player in mediating impairments in hippocampal-dependent associative plasticity upon sleep deprivation. This paper will review the role of the p75NTR, critically discuss the impact and implications of this research as the bridge for sleep research and neurological diseases.
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