Hypoxic Preconditioning Improves Spatial Cognitive Ability in Mice

Shao, Guo; Zhang, Ran; Wang, Zhanli; Gao, Chong; Huo, Xia; Lu, Guowei

doi:10.1159/000121368

Cited by 24 publications

(12 citation statements)

References 49 publications

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“…Whereas another study reported that hypoxia can improve memory in normal animals [22], we found that normal rats showed no significant enhancement of either spatial learning and memory or newborn cell activity following IH. This inconsistency may reflect the use of a different learning and memory task, BrdU dose and injection protocol, and species.…”

Section: Discussioncontrasting

confidence: 99%

Intermittent Hypoxia after Transient Focal Ischemia Induces Hippocampal Neurogenesis and c-Fos Expression and Reverses Spatial Memory Deficits in Rats

Tsai¹,

Yang²,

Wang³

et al. 2011

PLoS ONE

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BackgroundMemory impairment is a frequent complication of brain ischemia. Neurogenesis is implicated in learning and memory and is regulated by the transcription factor c-Fos. Preconditioning intermittent hypoxia (IH) attenuates ischemia-related memory impairments, but it is not known whether post-ischemia IH intervention has a similar effect. We investigated the effects of post-ischemia IH on hippocampal neurogenesis and c-Fos expression as well as spatial learning and memory in rats.Methodology/Principal FindingsFocal cerebral ischemia was induced in some rats by middle cerebral artery occlusion (MCAO), while other rats received sham MCAO surgery. Beginning a week later, half of the rats of each group received IH interventions (12% oxygen concentration, 4 hrs/d, for 7 d) and half received sham IH sessions. An additional group of rats received MCAO, IH, and injections of the neurogenesis-impairing agent 3′-AZT. Spatial learning and memory was measured in the Morris water maze, and hippocampal neurogenesis and c-Fos expression were examined. Hypoxia-inducible factor 1α (HIF-1α) and phosphorylated mitogen-activated protein kinase (pMAPK) were considered as possible mediators of IH-induced changes in neurogenesis and c-Fos expression. IH intervention following MCAO resulted in recovered spatial memory, increased hippocampal neurogenesis, and increased expression of c-Fos in newborn hippocampal cells. These effects were blocked by 3′-AZT. IH intervention following MCAO also was associated with increased hippocampal pMAPK and HIF-1α expression.Conclusions/SignificanceIH intervention following MCAO rescued ischemia-induced spatial learning and memory impairments, likely by inducing hippocampal neurogenesis and c-Fos expression through mediators including pMAPK and HIF-1α

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Section: Discussioncontrasting

confidence: 99%

Intermittent Hypoxia after Transient Focal Ischemia Induces Hippocampal Neurogenesis and c-Fos Expression and Reverses Spatial Memory Deficits in Rats

Tsai¹,

Yang²,

Wang³

et al. 2011

PLoS ONE

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“…The procedure of hypoxic experiment was performed as previously described [9]. The mice were placed into a 125 mL jar with fresh air, which was sealed with a rubber plug.…”

Section: Methodsmentioning

confidence: 99%

“…After sacrifice, the brain was quickly removed and placed in ice-cold, oxygenated artificial cerebrospinal fluid (ACSF) for about one minute. The hippocampal slices were prepared essentially as previously indicated [9]. Freshly prepared slices were maintained in ACSF at room temperature for at least 3 h before recording.…”

Section: Methodsmentioning

confidence: 99%

“…The salient aspect of this animal model is that the tolerance to hypoxia is increased with each exposure, and functions in an essentially linear arithmetic progression [7]. Using this model we have observed changes in molecules of the brain, including hypoxia-inducible factor (HIF)-1α, in developing hypoxic preconditioning in autoprogressive hypoxia [7,8,9]. We propose that HIF-1α can play an important role in contributing to neuron protection [7].…”

Section: Introductionmentioning

confidence: 99%

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The Effects of CoCl2 on HIF-1α Protein under Experimental Conditions of Autoprogressive Hypoxia Using Mouse Models

Zhang

Wang

Meister

et al. 2014

IJMS

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It is well known that cobalt chloride (CoCl2) can enhance the stability of hypoxia-inducible factor (HIF)-1α. The aim of this study is to detect the effect of CoCl2 on the hypoxia tolerance of mice which were repeatedly exposed to autoprogressive hypoxia. Balb/c mice were randomly divided into groups of chemical pretreatment and normal saline (NS), respectively injected with CoCl2 and NS 3 h before exposure to hypoxia for 0 run (H0), 1 run (H1), and 4 runs (H4). Western Blot, electrophoretic mobility shift assay (EMSA), extracellular recordings population spikes in area cornus ammonis I (CA 1) of mouse hippocampal slices and real-time were used in this study. Our results demonstrated that the tolerance of mice to hypoxia, the changes of HIF-1α protein level and HIF-1 DNA binding activity in mice hippocampus, the mRNA level of erythropoietin (EPO) and vascular endothelial growth factor (VEGF), and the disappearance time of population spikes of hippocampal slices were substantially different between the control group and the CoCl2 group. Over-induction of HIF-1α by pretreatment with CoCl2 before hypoxia did not increase the hypoxia tolerance.

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“…The procedure for hypoxic exposure was performed as previously described [ 17 ]. Briefly, the male mice were placed into a 125 mL jar with fresh air, and the jar was sealed with a rubber plug.…”

Section: Methodsmentioning

confidence: 99%

Hypoxia, hibernation and Neuroprotection: An Experimental Study in Mice

Ren¹,

Li²,

Rajah

et al. 2018

Aging and disease

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Hibernation is a unique physiological state that evolved to survive periods of food shortages. It is characterized by profound decreases in metabolic rate, body temperature and physiological functions. Studies have shown that animals in hibernation can resist neurological damage. Here, we aimed to study whether hypoxia can induce a hibernation-like state in a traditionally non-hibernating animal and whether it is neuroprotective. All procedures were conducted according to international guidelines on laboratory animal safety. Mice C57BL/6 (19-21g) were placed into a 125 mL jar with fresh air and the jar was sealed with a rubber plug. For each run, the tolerance limit was judged by the animals’ appearance for "air hunger”. The animal was removed from the jar as soon as its first gasping breath appeared and was moved to another fresh-air-containing jar of similar volume. This procedure was performed in four runs. The hypoxia exposure significantly decreased oxygen (O2) consumption, carbon dioxide (CO2) production, respiratory rate and heart rate. Meanwhile, rectal temperature reached a minimum of 12.7±2.56°C, which is lower than a wide range of ambient temperatures. The mimicked hibernation decreased the infarct size in a focal cerebral ischemia mouse model. Our findings suggest the possibility of inducing suspended animation-like hibernation states for medical applications post injury.

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Hypoxic Preconditioning Improves Spatial Cognitive Ability in Mice

Cited by 24 publications

References 49 publications

Intermittent Hypoxia after Transient Focal Ischemia Induces Hippocampal Neurogenesis and c-Fos Expression and Reverses Spatial Memory Deficits in Rats

Intermittent Hypoxia after Transient Focal Ischemia Induces Hippocampal Neurogenesis and c-Fos Expression and Reverses Spatial Memory Deficits in Rats

The Effects of CoCl2 on HIF-1α Protein under Experimental Conditions of Autoprogressive Hypoxia Using Mouse Models

Hypoxia, hibernation and Neuroprotection: An Experimental Study in Mice

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