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记忆印迹上的糖皮质激素印记。

The glucocorticoid footprint on the memory engram.

作者信息

Jeanneteau Freddy, Coutellier Laurence

机构信息

Institut de Génomique Fonctionnelle, University of Montpellier, INSERM, CNRS, Montpellier, France.

Departments of Psychology and Neuroscience, Ohio State University, Columbus, USA.

出版信息

Curr Opin Endocr Metab Res. 2022 Aug;25. doi: 10.1016/j.coemr.2022.100378. Epub 2022 Jun 20.

DOI:10.1016/j.coemr.2022.100378
PMID:38486965
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10938917/
Abstract

The complexity of the classical inverted U-shaped relationship between cortisol levels and responses transposable to stress reactivity has led to an incomplete understanding of the mechanisms enabling healthy and toxic effects of stress on brain and behavior. A clearer, more detailed, picture of those relationships can be obtained by integrating cortisol effects on large-scale brain networks, in particular, by focusing on neural network configurations from the perspective of inhibition and excitation. A unifying view of Semon and Hebb's theories of cellular memory links the biophysical and metabolic changes in neuronal ensembles to the strengthening of collective synapses. In that sense, the neuronal capacity to record, store, and retrieve information directly relates to the adaptive capacity of its connectivity and metabolic reserves. Here, we use task-activated cell ensembles or simply engram cells as an example to demonstrate that the adaptive behavioral responses to stress result from collective synapse strength within and across networks of interneurons and excitatory ones.

摘要

皮质醇水平与可转化为应激反应性的反应之间经典的倒U形关系十分复杂,这导致人们对压力对大脑和行为产生健康和有害影响的机制理解不完整。通过整合皮质醇对大规模脑网络的影响,特别是从抑制和兴奋的角度关注神经网络配置,可以更清晰、更详细地了解这些关系。对西蒙和赫布细胞记忆理论的统一观点将神经元集合中的生物物理和代谢变化与集体突触的强化联系起来。从这个意义上说,神经元记录、存储和检索信息的能力与其连接性和代谢储备的适应能力直接相关。在这里,我们以任务激活的细胞集合或简单的记忆印迹细胞为例,证明对应激的适应性行为反应源于中间神经元和兴奋性神经元网络内部及之间的集体突触强度。

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Neuron. 2022 May 4;110(9):1450-1467. doi: 10.1016/j.neuron.2022.02.020. Epub 2022 Mar 21.
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Negative Allosteric Modulation of Gamma-Aminobutyric Acid A Receptors at α5 Subunit-Containing Benzodiazepine Sites Reverses Stress-Induced Anhedonia and Weakened Synaptic Function in Mice.
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Psychoneuroendocrinology. 2022 Feb;136:105607. doi: 10.1016/j.psyneuen.2021.105607. Epub 2021 Nov 27.
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