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复发性呼吸暂停可诱导豚鼠前脑神经元凋亡。

Recurrent apnea induces neuronal apoptosis in the guinea pig forebrain.

作者信息

Zhang Jian-Hua, Fung Simon J, Xi Mingchu, Sampogna Sharon, Chase Michael H

机构信息

WebSciences International, Los Angeles, CA 90024, USA.

出版信息

Exp Neurol. 2009 Apr;216(2):290-4. doi: 10.1016/j.expneurol.2008.12.003. Epub 2008 Dec 16.

Abstract

Obstructive sleep apnea (OSA) and sleep-disordered breathing (SDB) can result in impaired cognition and mental acuity, and the generation of mood disorders, including depression. However, the mechanisms of neuronal damage for these complications have not been elucidated. Accordingly, using immunohistochemical technique with monoclonal antibody against single-stranded DNA, we examined the morphological effects of chronic recurrent apnea on neurons in the hippocampus and related forebrain sites in guinea pigs. Our results show that a large number of neurons labeled by anti-ssDNA antibody were present in the cingulate, insular and frontal cortices, the hippocampus and the amygdala in conjunction with periods of recurrent apnea. However, no labeling was observed in comparable regions of the brain in control guinea pigs. In the cortices of experimental animals, labeled neurons were detected mainly in the superficial layers (II-III) in the frontal, insular and cingulate cortex. In the hippocampus, most labeled neurons were located in the CA1 region, in which most of stained neurons were observed in strata pyramidal, while only a few positive neurons were located in the strata radiatum and the strata oriens. In addition, a large number of labeled neurons were also detected in the central nucleus of amygdala in the guinea pigs underwent recurrent periods of apnea. The present data indicate that recurrent apnea results in cell death in the hippocampus and related forebrain regions via mechanisms of apoptosis, which may represent the basis for the clinical complications of obstructive sleep apnea and sleep-disordered breathing.

摘要

阻塞性睡眠呼吸暂停(OSA)和睡眠呼吸紊乱(SDB)可导致认知功能和精神敏锐度受损,并引发包括抑郁症在内的情绪障碍。然而,这些并发症的神经元损伤机制尚未阐明。因此,我们使用针对单链DNA的单克隆抗体的免疫组织化学技术,研究了慢性反复呼吸暂停对豚鼠海马体及相关前脑部位神经元的形态学影响。我们的结果表明,在反复呼吸暂停期间,扣带回、岛叶和额叶皮质、海马体和杏仁核中存在大量被抗单链DNA抗体标记的神经元。然而,在对照豚鼠大脑的类似区域未观察到标记。在实验动物的皮质中,标记的神经元主要在额叶、岛叶和扣带回皮质的浅层(II-III层)被检测到。在海马体中,大多数标记的神经元位于CA1区域,其中大多数染色神经元在锥体细胞层被观察到,而只有少数阳性神经元位于辐射层和原层。此外,在经历反复呼吸暂停的豚鼠杏仁核中央核中也检测到大量标记的神经元。目前的数据表明,反复呼吸暂停通过凋亡机制导致海马体及相关前脑区域的细胞死亡,这可能是阻塞性睡眠呼吸暂停和睡眠呼吸紊乱临床并发症的基础。

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