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[记忆的神经机制:突触假说与基因组假说]

[Neural mechanisms of memory: synaptic and genomic hypotheses].

作者信息

Arshavskiĭ Iu I

出版信息

Zh Vyssh Nerv Deiat Im I P Pavlova. 2011 Nov-Dec;61(6):660-74.

Abstract

Memorizing of new facts and events means that entering signals produce definite changes within the brain. According to the commonly accepted hypothesis, traces of memory are stored through modifications in the strength of synaptic connections, resulting in formations of new patterns of neural activity. This synaptic hypothesis of memory determines the main direction of experimental studies in the field. It is shown in this review that the synaptic hypothesis can hardly explain the mechanism of long-term (often life-long) memory storage as well as memory resistance to both uncontrolled synaptic activity (epileptic seizures) and various adverse effects on the brain (anesthesia, injury, concussion, etc.). Arguments for an alternative hypothesis are given that long-term memory is mainly formed at the intraneural level through modifications of DNA molecules and associated proteins. This genomic hypothesis allows for a new approach to understanding the etiology ofAlzheimer's disease, whose initial symptom is solely memory impairment.

摘要

对新事实和事件的记忆意味着传入信号在大脑内产生明确的变化。根据普遍接受的假说,记忆痕迹是通过突触连接强度的改变来存储的,从而形成新的神经活动模式。这种记忆的突触假说决定了该领域实验研究的主要方向。本综述表明,突触假说很难解释长期(通常是终生)记忆存储的机制,以及记忆对不受控制的突触活动(癫痫发作)和大脑各种不利影响(麻醉、损伤、脑震荡等)的抵抗力。文中给出了另一种假说的论据,即长期记忆主要是通过DNA分子和相关蛋白质的修饰在神经内水平形成的。这种基因组假说为理解阿尔茨海默病的病因提供了一种新方法,其最初症状仅仅是记忆障碍。

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