短期缺氧影响嗅觉灵敏度的可能机制

E. Bezgacheva, E. Bigdaj
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摘要

文章的重点是短期缺氧对嗅觉灵敏度的影响。通过测定正丁醇的阈值,研究了短期缺氧对人类和大鼠嗅觉灵敏度的影响。结果表明,氧分压降低会导致嗅觉灵敏度下降。众所周知,气味检测阈值是受体细胞功能状态的表征。可以推测,在缺氧情况下,嗅觉感知过程缺乏能量供应可能会导致其灵敏度降低。为了验证这一假设,我们在鱼藤酮模型中用正丁醇刺激了大鼠的嗅觉神经元。根据 B. Chance 方法,通过改变还原吡啶核苷酸(NADH)的内在荧光强度来评估嗅觉神经元的细胞呼吸反应。结果分析表明,在常氧条件下,嗅觉神经元受到气味刺激后,NADH 荧光强度会增加,这表明线粒体中吡啶核苷酸还原形式的积累,从而表明细胞呼吸因接触气味而被激活。在鱼藤酮引起的缺氧情况下,NADH 的荧光诱导变化要么没有增加,要么反应幅度减半。这说明,气味导致的 NADH 恢复要么根本没有发生,要么对气味的反应明显低于正常缺氧时的反应,这表明缺氧时细胞呼吸减弱。这就是 ATP 合成减少的原因,而 ATP 合成减少会影响嗅觉传导过程的效率和嗅觉感觉神经元的灵敏度。因此,根据我们的研究结果可以得出结论,缺氧导致大鼠和人类嗅觉灵敏度减弱的原因可能是嗅觉神经元的细胞呼吸作用减弱。
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POSSIBLE MECHANISM OF INFLUENCE OF SHORT-TERM HYPOXIA ON OLFACTORY SENSITIVITY
The article is focused on the effect of short-term hypoxia on the olfactory sensitivity. The effect of short-term hypoxia on the olfactory sensitivity in human and rats were studied by determination thresholds for n-butanol. We have shown that reduced oxygen partial pressure leads to reduction of olfactory sensitivity. As known, odorant detection thresholds characterize the functional state of receptor cells. It can be assumed that the weakening of their sensitivity may be caused by a lack of energy supply to the olfactory perception process in hypoxia. To test this hypothesis, we stimulated rat olfactory sensory neurons with n-butanol in rotenone model. The reaction of cellular respiration of olfactory sensory neurons was evaluated by changing the intensity of intrinsic fluorescence of reduced pyridine nucleotides (NADH) according to the B. Chance method. Analysis of the results showed that under normoxia, stimulation of olfactory neurons by odorant caused an increase in the intensity of NADH fluorescence, which indicates the accumulation of the reduced form of pyridine nucleotides in mitochondria, and, consequently, the activation of cellular respiration due to exposure to odorant. In hypoxia caused by rotenone, an increase in the induced change of fluorescence of NADH was either not registered or the amplitude of the reaction was halved. This means that the recovery of NADH due to the odorant either did not occur at all, or this reaction to the smell was significantly lower than with normoxia, which indicates a weakening of cellular respiration during hypoxia. This is the reason for the decrease in ATP synthesis, which affects the efficiency of the olfactory transduction process and the sensitivity of olfactory sensory neurons. Therefore, based on our results, it can be concluded that the weakening of olfactory sensitivity in rats and humans with hypoxia may be due to a weakening of cellular respiration in olfactory sensory neurons.
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