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慢性行为应激会诱导内侧前额叶皮质锥体神经元的顶端树突发生重组。

Chronic behavioral stress induces apical dendritic reorganization in pyramidal neurons of the medial prefrontal cortex.

作者信息

Radley J J, Sisti H M, Hao J, Rocher A B, McCall T, Hof P R, McEwen B S, Morrison J H

机构信息

Kastor Neurobiology of Aging Laboratories and Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, NY 10029, USA.

出版信息

Neuroscience. 2004;125(1):1-6. doi: 10.1016/j.neuroscience.2004.01.006.

Abstract

Both the hippocampus and the medial prefrontal cortex (mPFC) play an important role in the negative feedback regulation of hypothalamic-pituitary-adrenal (HPA) activity during physiologic and behavioral stress. Moreover, chronic behavioral stress is known to affect the morphology of CA3c pyramidal neurons in the rat, by reducing total branch number and length of apical dendrites. In the present study, we investigated the effects of behavioral stress on the mPFC, using the repeated restraint stress paradigm. Animals were perfused after 21 days of daily restraint, and intracellular iontophoretic injections of Lucifer Yellow were carried out in pyramidal neurons of layer II/III of the anterior cingulate cortex and prelimbic area. Cellular reconstructions were performed on apical and basal dendrites of pyramidal neurons in layer II/III of the anterior cingulate and prelimbic cortices. We observed a significant reduction on the total length (20%) and branch numbers (17%) of apical dendrites, and no significant reduction in basal dendrites. These cellular changes may impair the capacity of the mPFC to suppress the response of the HPA axis to stress, and offer an experimental model of stress-induced neocortical reorganization that may provide a structural basis for the cognitive impairments observed in post-traumatic stress disorder.

摘要

海马体和内侧前额叶皮质(mPFC)在生理和行为应激期间下丘脑-垂体-肾上腺(HPA)活动的负反馈调节中均发挥着重要作用。此外,已知慢性行为应激会通过减少大鼠CA3c锥体神经元顶树突的总分支数和长度来影响其形态。在本研究中,我们使用重复束缚应激范式研究了行为应激对mPFC的影响。在每日束缚21天后对动物进行灌注,并在前扣带回皮质和前额叶前区的II/III层锥体神经元中进行细胞内离子电泳注射荧光黄。对前扣带回和前额叶前区II/III层锥体神经元的顶树突和基底树突进行细胞重建。我们观察到顶树突的总长度(20%)和分支数(17%)显著减少,而基底树突没有显著减少。这些细胞变化可能会损害mPFC抑制HPA轴对应激反应的能力,并提供一个应激诱导的新皮质重组的实验模型,这可能为创伤后应激障碍中观察到的认知障碍提供结构基础。

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