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压力对抑制性神经回路的影响，我们对布鲁斯·麦克尤恩的致敬。

Impact of stress on inhibitory neuronal circuits, our tribute to Bruce McEwen.

作者信息

Perez-Rando Marta, Carceller Hector, Castillo-Gomez Esther, Bueno-Fernandez Clara, García-Mompó Clara, Gilabert-Juan Javier, Guirado Ramón, Pesarico Ana Paula, Nacher Juan

机构信息

Neurobiology Unit, Program in Neurosciences and Institute of Biotechnology and Biomedicine (BIOTECMED), Universitat de València, Burjassot, Spain.

Spanish National Network for Research in Mental Health, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Madrid, Spain.

出版信息

Neurobiol Stress. 2022 May 13;19:100460. doi: 10.1016/j.ynstr.2022.100460. eCollection 2022 Jul.

DOI:10.1016/j.ynstr.2022.100460
PMID:35734023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9207718/
Abstract

This manuscript is dedicated to the memory of Bruce S. McEwen, to commemorate the impact he had on how we understand stress and neuronal plasticity, and the profound influence he exerted on our scientific careers. The focus of this review is the impact of stressors on inhibitory circuits, particularly those of the limbic system, but we also consider other regions affected by these adverse experiences. We revise the effects of acute and chronic stress during different stages of development and lifespan, taking into account the influence of the sex of the animals. We review first the influence of stress on the physiology of inhibitory neurons and on the expression of molecules related directly to GABAergic neurotransmission, and then focus on specific interneuron subpopulations, particularly on parvalbumin and somatostatin expressing cells. Then we analyze the effects of stress on molecules and structures related to the plasticity of inhibitory neurons: the polysialylated form of the neural cell adhesion molecule and perineuronal nets. Finally, we review the potential of antidepressants or environmental manipulations to revert the effects of stress on inhibitory circuits.

摘要

本手稿谨献给布鲁斯·S·麦克尤恩，以纪念他对我们理解压力和神经元可塑性所产生的影响，以及他对我们科学事业所施加的深远影响。本综述的重点是应激源对抑制性回路的影响，特别是边缘系统的抑制性回路，但我们也会考虑受这些不良经历影响的其他区域。我们探讨了在发育和生命周期的不同阶段急性和慢性应激的影响，同时考虑了动物性别的影响。我们首先回顾应激对抑制性神经元生理学以及与GABA能神经传递直接相关分子表达的影响，然后聚焦于特定的中间神经元亚群，特别是表达小白蛋白和生长抑素的细胞。接着我们分析应激对与抑制性神经元可塑性相关的分子和结构的影响：神经细胞黏附分子的多唾液酸化形式和神经元周围网。最后，我们综述抗抑郁药或环境干预逆转应激对抑制性回路影响的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5662/9207718/657f54fc13de/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5662/9207718/657f54fc13de/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5662/9207718/657f54fc13de/gr1.jpg

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Acute Ketamine Facilitates Fear Memory Extinction in a Rat Model of PTSD Along With Restoring Glutamatergic Alterations and Dendritic Atrophy in the Prefrontal Cortex.急性氯胺酮可促进创伤后应激障碍大鼠模型中的恐惧记忆消退，并恢复前额叶皮层的谷氨酸能改变和树突萎缩。
Front Pharmacol. 2022 Mar 17;13:759626. doi: 10.3389/fphar.2022.759626. eCollection 2022.
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