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严重的应激激素状况会导致小鼠基底外侧杏仁核的兴奋性窗口延长。

Severe stress hormone conditions cause an extended window of excitability in the mouse basolateral amygdala.

作者信息

Karst Henk, Joëls Marian

机构信息

Dept. Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, The Netherlands.

Dept. Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, The Netherlands.

出版信息

Neuropharmacology. 2016 Nov;110(Pt A):175-180. doi: 10.1016/j.neuropharm.2016.07.027. Epub 2016 Jul 25.

Abstract

Shortly after stress, basolateral amygdala neurons are exposed to sequential yet partly overlapping waves of hormones. We examined how these hormonal waves can change activity of basolateral amygdala neurons such that emotional aspects of stress become so deeply ingrained. To this end, spontaneous glutamatergic transmission was recorded during and up to several hours after combined adrenergic and corticosteroid waves, targeting the time-window relevant for encoding of stress-related information. Hormonal waves mimicking moderately stressful conditions cause a transient enhancement followed by later suppression of glutamatergic transmission. However, this late phase flips from suppressed to enhanced glutamatergic transmission with conditions mimicking severe stress. Such a prolonged window of enhanced excitability may contribute to the excessively strong encoding seen after the experience of highly stressful or traumatic events.

摘要

应激后不久,基底外侧杏仁核神经元会暴露于一系列相继但部分重叠的激素浪潮中。我们研究了这些激素浪潮如何改变基底外侧杏仁核神经元的活动,从而使应激的情绪方面得以深深烙印。为此,在肾上腺素能和皮质类固醇激素浪潮期间及之后数小时记录自发性谷氨酸能传递,目标是与应激相关信息编码相关的时间窗口。模拟中度应激条件的激素浪潮会导致谷氨酸能传递先短暂增强,随后受到抑制。然而,在模拟严重应激的条件下,这个后期阶段会从谷氨酸能传递受抑制转变为增强。这种兴奋性增强的延长窗口可能导致在经历高度应激或创伤性事件后出现过度强烈的编码。

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