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抑郁症单胺能理论中的锌:其与神经可塑性的关系。

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity.

作者信息

Doboszewska Urszula, Wlaź Piotr, Nowak Gabriel, Radziwoń-Zaleska Maria, Cui Ranji, Młyniec Katarzyna

机构信息

Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, 30-688 Kraków, Poland; Department of Animal Physiology, Institute of Biology and Biochemistry, Faculty of Biology and Biotechnology, Maria Curie-Sklodowska University, Akademicka 19, 20-033 Lublin, Poland.

Department of Animal Physiology, Institute of Biology and Biochemistry, Faculty of Biology and Biotechnology, Maria Curie-Sklodowska University, Akademicka 19, 20-033 Lublin, Poland.

出版信息

Neural Plast. 2017;2017:3682752. doi: 10.1155/2017/3682752. Epub 2017 Feb 19.

DOI:10.1155/2017/3682752
PMID:28299207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5337390/
Abstract

Preclinical and clinical studies have demonstrated that zinc possesses antidepressant properties and that it may augment the therapy with conventional, that is, monoamine-based, antidepressants. In this review we aim to discuss the role of zinc in the pathophysiology and treatment of depression with regard to the monoamine hypothesis of the disease. Particular attention will be paid to the recently described zinc-sensing GPR39 receptor as well as aspects of zinc deficiency. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity.

摘要

临床前和临床研究表明,锌具有抗抑郁特性,并且可能增强传统的(即基于单胺的)抗抑郁药的治疗效果。在本综述中,我们旨在讨论锌在抑郁症的病理生理学和治疗中的作用,这与该疾病的单胺假说有关。将特别关注最近描述的锌感应GPR39受体以及锌缺乏的方面。此外,我们将尝试对锌在抑郁症和神经可塑性背景下与单胺系统相互作用的机制给出一个可能的解释。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd2/5337390/21481e2d5246/NP2017-3682752.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd2/5337390/21481e2d5246/NP2017-3682752.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edd2/5337390/21481e2d5246/NP2017-3682752.001.jpg

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Neuropharmacology. 2016 Dec;111:242-252. doi: 10.1016/j.neuropharm.2016.09.011. Epub 2016 Sep 12.
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Behavioral Abnormality Induced by Enhanced Hypothalamo-Pituitary-Adrenocortical Axis Activity under Dietary Zinc Deficiency and Its Usefulness as a Model.膳食锌缺乏下下丘脑-垂体-肾上腺皮质轴活动增强诱导的行为异常及其作为模型的效用
Int J Mol Sci. 2016 Jul 16;17(7):1149. doi: 10.3390/ijms17071149.
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Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells.
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Arch Toxicol. 2025 Jan;99(1):23-41. doi: 10.1007/s00204-024-03891-3. Epub 2024 Nov 7.
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The CB2-PKC pathway is involved in esketamine-induced anti-inflammation in BV-2 microglial cells exposed to lipopolysaccharides.CB2-PKC通路参与了艾氯胺酮对暴露于脂多糖的BV-2小胶质细胞的抗炎作用。
Am J Transl Res. 2024 Sep 15;16(9):4466-4478. doi: 10.62347/RRZF5229. eCollection 2024.
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