POSSIBLE MECHANISM OF INFLUENCE OF SHORT-TERM HYPOXIA ON OLFACTORY SENSITIVITY-Reference-Cited by-同舟云学术

POSSIBLE MECHANISM OF INFLUENCE OF SHORT-TERM HYPOXIA ON OLFACTORY SENSITIVITY

Published:2024-05-21 Issue:2 Volume:8 Page:207-211
ISSN:2499-9962
Container-title:Russian Journal of Biological Physics and Chemisrty
language:en
Short-container-title:

Author:

Bezgacheva E.¹,Bigdaj E.²³

Affiliation:

1. Kirov Military medical academy

2. Saint-Petersburg State Pediatric Medical University

3. Pavlov Institute of Physiology RAS

Abstract

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.

Publisher

RIOR Publishing Center

Reference19 articles.

1. Son G. et al. Olfactory neuropathology in Alzheimer’s disease: A sign of ongoing neurodegeneration. BMB reports, 2021, vol. 54, no. 6, p. 295, doi: 10.5483/BMBRep.2021.54.6.055., Son G. et al. Olfactory neuropathology in Alzheimer’s disease: A sign of ongoing neurodegeneration. BMB reports, 2021, vol. 54, no. 6, p. 295, doi: 10.5483/BMBRep.2021.54.6.055.

2. Hawkes C. Olfaction in neurodegenerative disorder. Taste and Smell, 2006, vol. 63, pp. 133-151., Hawkes C. Olfaction in neurodegenerative disorder. Taste and Smell, 2006, vol. 63, pp. 133-151.

3. Hawkes C.H., Shephard B.C. Selective anosmia in Parkinson's disease? The Lancet, 1993, vol. 341, no. 8842, pp. 435-436., Hawkes C.H., Shephard B.C. Selective anosmia in Parkinson's disease? The Lancet, 1993, vol. 341, no. 8842, pp. 435-436.

4. Peers C., Pearson H.A., Boyle J.P. Hypoxia and Alzheimer’s disease. Essays in biochemistry, 2007, vol. 43, pp. 153-164., Peers C., Pearson H.A., Boyle J.P. Hypoxia and Alzheimer’s disease. Essays in biochemistry, 2007, vol. 43, pp. 153-164.

5. Chen G.J. et al. Transient hypoxia causes Alzheimer-type molecular and biochemical abnormalities in cortical neurons: potential strategies for neuroprotection. Journal of Alzheimer's Disease, 2003, vol. 5, no. 3, pp. 209-228., Chen G.J. et al. Transient hypoxia causes Alzheimer-type molecular and biochemical abnormalities in cortical neurons: potential strategies for neuroprotection. Journal of Alzheimer's Disease, 2003, vol. 5, no. 3, pp. 209-228.