Insight into potential mechanisms of hypobaric hypoxia–induced learning and memory deficit – Lessons from rat studies

Qaid, Entesar Yaseen Abdo; Zakaria, Rahimah; Sulaiman, Shaida Fariza; Yusof, Nurul Aiman Mohd; Shafin, Nazlahshaniza; Othman, Zahiruddin; Ahmad, Asma Hayati; Aziz, Cb Abd

doi:10.1177/0960327116689714

Cited by 21 publications

(12 citation statements)

References 93 publications

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“…It has been shown that HH can shorten escape latency and target quadrant residence time, and reduce the number of crossings of the target quadrant in the MWM, which suggests that spatial learning and memory ability are reduced. [1,3,17] In accordance with previous studies, we found that after 5 days of acquisition training, the ability of all of the rats to locate the platform had improved. However, compared with rats housed in a normobaric normoxia environment, rats exposed to HH for 4 weeks had a significantly longer escape latency ( P < 0.05), while there was no significant between-group difference in the average swimming speed.…”

Section: Discussionsupporting

confidence: 90%

“…In particular, the hippocampus, EC, striatum, thalamus, and basal forebrain play important roles in cognition. [17–20] Although an increasing number of pathophysiological and MRI studies involve the evaluation of brain regions other than just the hippocampus, extensive histological analysis of the whole brain is unrealistic. Therefore, it is necessary to evaluate changes of cognitive function caused by HH exposure objectively and comprehensively.…”

Section: Discussionmentioning

confidence: 99%

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Abnormal brain activity in rats with sustained hypobaric hypoxia exposure

Yuan

Wang

Liu

et al. 2019

Chinese Medical Journal

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Background:Hypobaric hypoxia (HH) exposure at high altitudes can result in a decline in cognitive function, which may have a serious impact on the daily life of people who migrate to high altitudes. However, the specific HH-induced changes in brain function remain unclear. This study explored changes in brain activity in rats exposed to a sustained HH environment using functional magnetic resonance imaging (fMRI).Methods:Healthy male rats (8 weeks old) were randomly divided into a model group and a control group. A rat model of cognitive impairment induced by sustained HH exposure was established. The control and model groups completed training and testing in the Morris water maze (MWM). A two-sample t-test for between-group difference comparisons was performed. Repeated measures analyses of variance for within-group comparisons were performed and post-hoc comparisons were made using the Tukey test. Between-group differences in spontaneous brain activity were assessed using a voxel-wise analysis of resting-state fMRI (rs-fMRI), combined with analyses of the fractional amplitude of low frequency fluctuations (fALFF) in statistical parametric mapping.Results:In the MWM test, the escape latencies of the model group were significantly longer compared with those of the control group (control group vs. model group, day 1: 21.6 ± 3.3 s vs. 40.5 ± 3.4 s, t = –11.282; day 2: 13.5 ± 2.2 s vs. 28.7 ± 5.3 s, t = –7.492; day 3: 10.5 ± 2.8 s vs. 22.6 ± 6.1 s, t = –5.099; day 4: 9.7 ± 2.5 s vs. 18.6 ± 5.2 s, t = –4.363; day 5: 8.8 ± 2.7 s vs. 16.7 ± 5.0 s, t = –3.932; all P < 0.001). Within both groups, the escape latency at day 5 was significantly shorter than those at other time points (control group: F = 57.317, P < 0.001; model group: F = 50.718, P < 0.001). There was no within-group difference in average swimming speed (control group, F = 1.162, P = 0.956; model group, F = 0.091, P = 0.880). Within the model group, the time spent within the original platform quadrant was significantly shorter (control group vs. model group: 36.1 ± 5.7 s vs. 17.8 ± 4.3 s, t = 7.249, P < 0.001) and the frequency of crossing the original platform quadrant was significantly reduced (control group vs. model group: 6.4 ± 1.9 s vs. 2.0 ± 0.8 s, t = 6.037, P < 0.001) compared with the control group. In the rs-fMRI study, compared with the control group, rats in the model group showed widespread reductions in fALFF values throughout the brain.Conclusions:The abnormalities in spontaneous brain activity indicated by the fALFF measurements may reflect changes in brain function after HH exposure. This widespread abnormal brain activity may help to explain and to provide new insights into the mechanism underlying the impairment of brain function under sustained exposure to high altitudes.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Abnormal brain activity in rats with sustained hypobaric hypoxia exposure

Yuan

Wang

Liu

et al. 2019

Chinese Medical Journal

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“…Moreover, the effects of hypoxia on the brain display region-specific characteristics [28,29]. We studied the effects of NBP on learning and memory functions [30,31], which commonly decline under these conditions, to evaluate the effects of this agent on cognitive ability. The effects of NBP on other cognitive functions under conditions of hypobaric hypoxia remain to be investigated.…”

Section: Discussionmentioning

confidence: 99%

DL-3-n-butylphthalide improved physical and learning and memory performance of rodents exposed to acute and chronic hypobaric hypoxia

Shi

Sun

et al. 2021

Military Med Res

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Background Studies have revealed the protective effect of DL-3-n-butylphthalide (NBP) against diseases associated with ischemic hypoxia. However, the role of NBP in animals with hypobaric hypoxia has not been elucidated. This study investigated the effects of NBP on rodents with acute and chronic hypobaric hypoxia. Methods Sprague-Dwaley rats and Kunming mice administered with NBP (0, 60, 120, and 240 mg/kg for rats and 0, 90, 180, and 360 mg/kg for mice) were placed in a hypobaric hypoxia chamber at 10,000 m and the survival percentages at 30 min were determined. Then, the time and distance to exhaustion of drug-treated rodents were evaluated during treadmill running and motor-driven wheel-track treadmill experiments, conducted at 5800 m for 3 days or 20 days, to evaluate changes in physical functions. The frequency of active escapes and duration of active escapes were also determined for rats in a shuttle-box experiment, conducted at 5800 m for 6 days or 27 days, to evaluate changes in learning and memory function. ATP levels were measured in the gastrocnemius muscle and malonaldehyde (MDA), superoxide dismutase (SOD), hydrogen peroxide (H2O2), glutathione peroxidase (GSH-Px), and lactate were detected in sera of rats, and routine blood tests were also performed. Results Survival analysis at 10,000 m indicated NBP could improve hypoxia tolerance ability. The time and distance to exhaustion for mice (NBP, 90 mg/kg) and time to exhaustion for rats (NBP, 120 and 240 mg/kg) significantly increased under conditions of acute hypoxia compared with control group. NBP treatment also significantly increased the time to exhaustion for rats when exposed to chronic hypoxia. Moreover, 240 mg/kg NBP significantly increased the frequency of active escapes under conditions of acute hypoxia. Furthermore, the levels of MDA and H2O2 decreased but those of SOD and GSH-Px in the sera of rats increased under conditions of acute and chronic hypoxia. Additionally, ATP levels in the gastrocnemius muscle significantly increased, while lactate levels in sera significantly decreased. Conclusion NBP improved physical and learning and memory functions in rodents exposed to acute or chronic hypobaric hypoxia by increasing their anti-oxidative capacity and energy supply.

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“…Grover 2012 12 quoted that withanolide A can be used both in treatment and prevention of Alzheimer's disease and associated pathology. Qaid et al, studied hypobaric hypoxia-induced memory deficit in rats 13 and Soman 2012 14 investigated the effect of Withania somnifera (WS) root extract and withanolide A (WD) in restoring spatial memory deficit by oxidative stress induced alteration in the hippocampus of epileptic rats and suggested treatment with WS and WA has ameliorated spatial memory deficits by enhancing antioxidant system and restoring altered N-methyl-D-aspartate receptor density.…”

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confidence: 99%

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2018

IJPSR

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Neurodegeneration is a powerful initiator for a number of nervous system related diseases that come under the term "neurodegenerative diseases". Neurodegenerative diseases are incurable, results in the progressive degeneration of nerve cells and causes problems with movement and mental functioning that became a challenge in present day's health care. For this study we made a model of Huntington's chorea, one of the neurodegenerative disorders by inducing experimental neurodegeneration and tried to prevent the neurodegeneration by giving ethanolic extract of Withania somnifera and its active principle withanolide A 10 days before the lesion surgery. The herb Withania somnifera is a well known herb in India and was used by all the Ayurvedic legends for nervous system related problems. We used 5 animal groups for this study they are CO, SC, LC, WS125 and WA100. All the animals were trained to walk in a narrow beam prior to surgery and were analyzed for motor coordination on the 5 th day post lesion to find out the protective nature of the drugs employed. The results were amazing. The behaviour of the drug group animals were more equivalent with the control animals unlike the LC animals, performed with lots of errors on beam walking. These results clearly indicates that the drugs were very good in protecting the nerve cells from experimental degeneration and so can do the same action in real life. INTRODUCTION: Neurons are the building blocks of the nervous system and normally they don't reproduce or replace themselves, so when they become damaged or die they cannot be replaced by the body. Huntington's disease (HD) is a neurodegenerative disorder that leads to progressive cell death mainly in the striatum, the main part of basal ganglia. Neychev et al., 2008 1 suggested that expression of dystonic movements depends on influences from basal ganglia by inducing lesions in striatum.

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Insight into potential mechanisms of hypobaric hypoxia–induced learning and memory deficit – Lessons from rat studies

Cited by 21 publications

References 93 publications

Abnormal brain activity in rats with sustained hypobaric hypoxia exposure

Abnormal brain activity in rats with sustained hypobaric hypoxia exposure

DL-3-n-butylphthalide improved physical and learning and memory performance of rodents exposed to acute and chronic hypobaric hypoxia

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