Hencz Alexandra Julia, Magony Andor, Thomas Chloe, Kovacs Krisztina, Szilagyi Gabor, Pal Jozsef, Sik Attila
Institute of Physiology, Medical School, University of Pécs, Pécs, Hungary.
Institute of Clinical Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Front Cell Neurosci. 2024 Apr 15;18:1376577. doi: 10.3389/fncel.2024.1376577. eCollection 2024.
Excess oxygen (O) levels may have a stimulating effect, but in the long term, and at high concentrations of O, it is harmful to the nervous system. The hippocampus is very sensitive to pathophysiological changes and altered O concentrations can interfere with hippocampus-dependent learning and memory functions. In this study, we investigated the hyperoxia-induced changes in the rat hippocampus to evaluate the short-term effect of mild and severe hyperoxia. Wistar male rats were randomly divided into control (21% O), mild hyperoxia (30% O), and severe hyperoxia groups (100% O). The O exposure lasted for 60 min. Multi-channel silicon probes were used to study network oscillations and firing properties of hippocampal putative inhibitory and excitatory neurons. Neural damage was assessed using the Gallyas silver impregnation method. Mild hyperoxia (30% O) led to the formation of moderate numbers of silver-impregnated "dark" neurons in the hippocampus. On the other hand, exposure to 100% O was associated with a significant increase in the number of "dark" neurons located mostly in the hilus. The peak frequency of the delta oscillation decreased significantly in both mild and severe hyperoxia in urethane anesthetized rats. Compared to normoxia, the firing activity of pyramidal neurons under hyperoxia increased while it was more heterogeneous in putative interneurons in the cornu ammonis area 1 (CA1) and area 3 (CA3). These results indicate that short-term hyperoxia can change the firing properties of hippocampal neurons and network oscillations and damage neurons. Therefore, the use of elevated O concentration inhalation in hospitals (i.e., COVID treatment and surgery) and in various non-medical scenarios (i.e., airplane emergency O masks, fire-fighters, and high altitude trekkers) must be used with extreme caution.
氧气(O)水平过高可能具有刺激作用,但从长期来看,高浓度的氧气对神经系统有害。海马体对病理生理变化非常敏感,氧气浓度的改变会干扰依赖海马体的学习和记忆功能。在本研究中,我们调查了高氧诱导的大鼠海马体变化,以评估轻度和重度高氧的短期影响。将雄性Wistar大鼠随机分为对照组(21% O)、轻度高氧组(30% O)和重度高氧组(100% O)。氧气暴露持续60分钟。使用多通道硅探针研究海马体假定的抑制性和兴奋性神经元的网络振荡和放电特性。使用Gallyas银浸染法评估神经损伤。轻度高氧(30% O)导致海马体中出现中等数量的银浸染“暗”神经元。另一方面,暴露于100% O与主要位于海马门的“暗”神经元数量显著增加有关。在乌拉坦麻醉的大鼠中,轻度和重度高氧条件下δ振荡的峰值频率均显著降低。与常氧相比,高氧条件下锥体神经元的放电活动增加,而在海马1区(CA1)和3区(CA3)假定的中间神经元中放电活动更加不均匀。这些结果表明,短期高氧可改变海马体神经元的放电特性和网络振荡并损伤神经元。因此,在医院(即新冠治疗和手术)以及各种非医疗场景(即飞机应急氧气面罩、消防员和高海拔徒步旅行者)中使用高浓度氧气吸入时必须极其谨慎。