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血清素能致幻剂如何治疗抑郁症:神经可塑性的潜在作用。

How do serotonergic psychedelics treat depression: The potential role of neuroplasticity.

作者信息

Artin Hewa, Zisook Sidney, Ramanathan Dhakshin

机构信息

Department of Psychiatry, UC San Diego, La Jolla, CA 92093, United States.

Department of Psychiatry, UC San Diego, San Diego, CA 92093, United States.

出版信息

World J Psychiatry. 2021 Jun 19;11(6):201-214. doi: 10.5498/wjp.v11.i6.201.

DOI:10.5498/wjp.v11.i6.201
PMID:34168967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8209538/
Abstract

Depression is a common mental disorder and one of the leading causes of disability around the world. Monoaminergic antidepressants often take weeks to months to work and are not effective for all patients. This has led to a search for a better understanding of the pathogenesis of depression as well as to the development of novel antidepressants. One such novel antidepressant is ketamine, which has demonstrated both clinically promising results and contributed to new explanatory models of depression, including the potential role of neuroplasticity in depression. Early clinical trials are now showing promising results of serotonergic psychedelics for depression; however, their mechanism of action remains poorly understood. This paper seeks to review the effect of depression, classic antidepressants, ketamine, and serotonergic psychedelics on markers of neuroplasticity at a cellular, molecular, electrophysiological, functional, structural, and psychological level to explore the potential role that neuroplasticity plays in the treatment response of serotonergic psychedelics.

摘要

抑郁症是一种常见的精神障碍,也是全球致残的主要原因之一。单胺能抗抑郁药通常需要数周甚至数月才能起效,而且并非对所有患者都有效。这促使人们更深入地了解抑郁症的发病机制,并研发新型抗抑郁药。氯胺酮就是这样一种新型抗抑郁药,它已展现出临床应用前景,并为抑郁症的新解释模型做出了贡献,包括神经可塑性在抑郁症中的潜在作用。早期临床试验目前显示血清素能致幻剂治疗抑郁症有良好效果;然而,其作用机制仍知之甚少。本文旨在综述抑郁症、经典抗抑郁药、氯胺酮和血清素能致幻剂在细胞、分子、电生理、功能、结构和心理层面上对神经可塑性标志物的影响,以探讨神经可塑性在血清素能致幻剂治疗反应中所起的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c86/8209538/bb597c01cfbb/WJP-11-201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c86/8209538/bb597c01cfbb/WJP-11-201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c86/8209538/bb597c01cfbb/WJP-11-201-g001.jpg

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Ketamine activated glutamatergic neurotransmission by GABAergic disinhibition in the medial prefrontal cortex.
艺术疗法与神经科学:证据、局限与误区
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The Psychedelic Future of Post-Traumatic Stress Disorder Treatment.创伤后应激障碍治疗的迷幻未来。
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Neuroimaging in psychedelic drug development: past, present, and future.神经影像学在迷幻药物研发中的应用:过去、现在和未来。
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