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靶向稳态突触可塑性治疗心境障碍。

Targeting Homeostatic Synaptic Plasticity for Treatment of Mood Disorders.

机构信息

Department of Pharmacology and the Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37240-7933, USA.

出版信息

Neuron. 2020 Jun 3;106(5):715-726. doi: 10.1016/j.neuron.2020.05.015.

DOI:10.1016/j.neuron.2020.05.015
PMID:32497508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7517590/
Abstract

Ketamine exerts rapid antidepressant action in depressed and treatment-resistant depressed patients within hours. At the same time, ketamine elicits a unique form of functional synaptic plasticity that shares several attributes and molecular mechanisms with well-characterized forms of homeostatic synaptic scaling. Lithium is a widely used mood stabilizer also proposed to act via synaptic scaling for its antimanic effects. Several studies to date have identified specific forms of homeostatic synaptic plasticity that are elicited by these drugs used to treat neuropsychiatric disorders. In the last two decades, extensive work on homeostatic synaptic plasticity mechanisms have shown that they diverge from classical synaptic plasticity mechanisms that process and store information and thus present a novel avenue for synaptic regulation with limited direct interference with cognitive processes. In this review, we discuss the intersection of the findings from neuropsychiatric treatments and homeostatic plasticity studies to highlight a potentially wider paradigm for treatment advance.

摘要

氯胺酮在数小时内就能对抑郁和治疗抵抗性抑郁患者产生快速的抗抑郁作用。与此同时,氯胺酮引发了一种独特的功能突触可塑性,它与经过充分研究的几种稳态突触可塑性形式具有几个相同的属性和分子机制。锂是一种广泛使用的心境稳定剂,也被认为通过突触可塑性发挥作用,具有抗躁狂作用。迄今为止,有几项研究确定了这些用于治疗神经精神疾病的药物所引发的特定形式的稳态突触可塑性。在过去的二十年中,对稳态突触可塑性机制的广泛研究表明,它们与处理和存储信息的经典突触可塑性机制不同,因此为突触调节提供了一种新的途径,对认知过程的直接干扰有限。在这篇综述中,我们讨论了神经精神疾病治疗和稳态可塑性研究结果的交集,以突出一个更广泛的治疗进展范例。

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