暴露于允许性高碳酸血症和/或常压缺氧后海马区CA1神经元的超微结构变化。

IF 3.6 4区 医学 Q3 CELL BIOLOGY Cellular and Molecular Neurobiology Pub Date : 2023-11-01 Epub Date: 2023-09-16 DOI:10.1007/s10571-023-01407-8
Pavel Tregub, Yuri Motin, Vladimir Kulikov, Pavel Kovzelev, Aleksandra Chaykovskaya, Irada Ibrahimli
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引用次数: 0

摘要

孤立暴露于间歇性缺氧和允许性高碳酸血症激活信号机制,诱导线粒体和内质网超微结构变化,并在这些因素的共同影响下,神经元产生最大的缺血耐受性。然而,这些因素对神经元细胞器超微结构的综合影响缺乏数据。本研究旨在比较评估单独和联合暴露于低氧和高碳酸血症后神经元的超微结构变化,并将这些变化与先前观察到的这些因素的神经保护潜力联系起来。在接受30分钟容许性高碳酸血症(PCO2≈50 mmHg)和/或正压缺氧(PO2≈150 mmHg) 15次治疗后,进行形态计量学评估,以评估海马神经元(线粒体、核周间隙和颗粒内质网)超微结构变化的程度。在CA1区的海马神经元中,允许性高碳酸血症导致线粒体大小增加,颗粒内质网膜室和核周间隙扩大。常压低氧仅影响线粒体大小,而高碳酸血症低氧特异性地使核周间隙变宽。这些超微结构变化客观反映了缺氧和高碳酸血症对神经元能量代谢、抗凋亡和合成功能等细胞器的不同程度的影响。这证实了它们在联合暴露下增强神经保护作用的作用,并强调了高碳酸盐成分在这一机制中的主导作用。
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Ultrastructural Changes in Hippocampal Region CA1 Neurons After Exposure to Permissive Hypercapnia and/or Normobaric Hypoxia.

Isolated exposure to intermittent hypoxia and permissive hypercapnia activates signaling mechanisms that induce ultrastructural changes in mitochondria and endoplasmic reticulum, accompanied by the development of maximal ischemic tolerance in neurons under the combined influence of these factors. However, there are a lack of data on the combined impact of these factors on the ultrastructure of neuronal organelles. The present study aims to comparatively assess the ultrastructural changes in neurons following isolated and combined exposure to hypoxia and hypercapnia, as well as to correlate these changes with the neuroprotective potential previously observed for these factors. Following a 15-session course of 30-min exposures to permissive hypercapnia (PCO2 ≈ 50 mmHg) and/or normobaric hypoxia (PO2 ≈ 150 mmHg), morphometric assessment was conducted to evaluate the extent of ultrastructural changes in hippocampal neurons (mitochondria, perinuclear space, and granular endoplasmic reticulum). It was found that in hippocampal neurons from the CA1 region, permissive hypercapnia resulted in increased mitochondrial size, expansion of membranous compartments of the granular endoplasmic reticulum, and perinuclear space. Normobaric hypoxia affected only mitochondrial size, while hypercapnic hypoxia specifically widened the perinuclear space. These ultrastructural changes objectively reflect varying degrees of the influence of hypoxia and hypercapnia on organelles responsible for energy metabolism, anti-apoptotic, and synthetic functions of neurons. This confirms the effect of potentiation of their neuroprotective effects under combined exposure and highlights the dominant role of the hypercapnic component in this mechanism.

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来源期刊
CiteScore
7.70
自引率
0.00%
发文量
137
审稿时长
4-8 weeks
期刊介绍: Cellular and Molecular Neurobiology publishes original research concerned with the analysis of neuronal and brain function at the cellular and subcellular levels. The journal offers timely, peer-reviewed articles that describe anatomic, genetic, physiologic, pharmacologic, and biochemical approaches to the study of neuronal function and the analysis of elementary mechanisms. Studies are presented on isolated mammalian tissues and intact animals, with investigations aimed at the molecular mechanisms or neuronal responses at the level of single cells. Cellular and Molecular Neurobiology also presents studies of the effects of neurons on other organ systems, such as analysis of the electrical or biochemical response to neurotransmitters or neurohormones on smooth muscle or gland cells.
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