Effect of oxidative stress induced by paradoxical sleep deprivation on the activities of Na+, K+-ATPase and acetylcholinesterase in the cortex and hippocampus of rat

Khadrawy, Yasser A.; Nour, Neveen A.; Ezz, Heba S. Aboul

doi:10.1016/j.trsl.2010.11.005

Cited by 42 publications

(32 citation statements)

References 72 publications

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“…Conversely, others have reported on the presence of increased oxidative stress in the hippocampus and cortex in sleep-deprived rats (74)(75)(76). The divergent reports are perhaps caused by the inherently different models of sleep deprivation used and also by the different brain regions being assessed.…”

Section: Discussionmentioning

confidence: 99%

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

Nair

Zhang

Ramesh

et al. 2011

Am J Respir Crit Care Med

154

138

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Rationale: Sleep fragmentation (SF) is one of the major characteristics of sleep apnea, and has been implicated in its morbid consequences, which encompass excessive daytime sleepiness and neurocognitive impairments. We hypothesized that absence of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity is neuroprotective in SF-induced cognitive impairments. Objectives: To examine whether increased NADPH oxidase activity may play a role in SF-induced central nervous system dysfunction. Methods: The effect of chronic SF during the sleep-predominant period on sleep architecture, sleep latency, spatial memory, and oxidative stress parameters was assessed in mice lacking NADPH oxidase activity (gp91phox-/Y ) and wild-type littermates. Measurements and Main Results: SF for 15 days was not associated with differences in sleep duration, sleep state distribution, or sleep latency in both gp91phox-/Y and control mice. However, on a standard place training task, gp91phox-/Y mice displayed normal learning and were protected from the spatial learning deficits observed in wildtype littermates exposed to SF. Moreover, anxiety levels were increased in wild-type mice exposed to SF, whereas no changes emerged in gp91phox-/Y mice. Additionally, wild-type mice, but not gp91phox-/Y mice, had significantly elevated NADPH oxidase gene expression and activity, and in malondialdehyde and 8-oxo-29-deoxyguanosine levels in cortical and hippocampal lysates after SF exposures. Conclusions: This work substantiates an important role for NADPH oxidase in hippocampal memory impairments induced by SF, modeling sleep apnea. Targeting NADPH oxidase, therefore, is expected to minimize hippocampal impairments from both intermittent hypoxia and SF associated with the disease. Keywords: NADPH oxidase; sleep fragmentation; neurocognitive impairmentsThe manifestations of obstructive sleep apnea (OSA) reflect the interactions of intermittent hypoxia (IH), intermittent hypercapnia, increased intrathoracic pressure swings, and sleep fragmentation (SF) as elicited by the episodic changes in upper airway resistance during sleep. SF is a common phenomenon among several clinical disorders, and can lead to impaired cognitive function via mechanisms that remain poorly understood (1). Indeed, uninterrupted sleep for a minimum length of time is required for optimal daytime vigilance and neurocognitive function (1-3). Preliminary studies in rodents using short-term SF paradigms have also confirmed the adverse effects of SF on learning and seem to be independent of adenosine-mediated synaptic inhibition (4-7).In clinical populations with severe SF (e.g., in OSA) total sleep time typically diminishes only slightly (8). The effects of experimentally induced SF on sleep patterns have not been critically characterized in rodents. It is likely that OSA-induced sleep perturbations are accompanied by obvious cognitive deficits because of increased levels of systemic markers of oxidative stress and inflammation, the latter leading to gray matter loss in neural...

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Section: Discussionmentioning

confidence: 99%

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

Nair

Zhang

Ramesh

et al. 2011

Am J Respir Crit Care Med

154

138

View full text Add to dashboard Cite

show abstract

“…The relationship between sleep deprivation and oxidative stress has been investigated in many studies, but the results are confl icting (42,43). Serum levels of nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine, and thiobarbituric acid reactive substances (TBARS) have not been found to differ signifi cantly between animals that were and were not sleep deprived.…”

Section: Discussionmentioning

confidence: 99%

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Saygın¹,

Özgüner²,

Önder³

et al. 2017

BLL

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BACKGROUND: To examine the impact of different types of sleep deprivation on hippocampal-mediated learning and memory in rats. METHODS: Forty-eight Sprague-Dawley male rats were randomly assigned to 1 of 4 equal-size groups: (1) 12 hours of sleep per day (control). (2) total sleep deprivation (TSD), (3) rapid eye movement (REM) deprivation (RD), and (4) sleep restricted to 4 hours per day (SR). All rats were subjected to swimming training in the Morris water maze (MWM). At the end of the experiments, the rats were decapitated, and hippocampus tissue was analyzed for several neurotransmitters and receptors. RESULTS: The time spent at the target quadrant increased from 20.2 to 30.0 seconds in the control group on the third day of the experiment, whereas corresponding values increased from 20.2 to 21.8 seconds in the TSD group, 22.1 to 25.4 seconds in the RD group, and 21.2 to 32.0 sec in the SR group (p = 0.026). On the seventh day of the experiment, the values decreased to 25.0 seconds in controls, 22.5 in the RD group, and 23.6 in the SR group (p = 0.045). The TSD group demonstrated signifi cant decreases in glutamate and serotonin levels compared with the control group. There was a signifi cant increase in 5-HT2 a receptor expression in all intervention groups compared with the controls. CONCLUSIONS: Our results of glutamate levels and 5-HT2a receptor expression in the hippocampus seem to be primarily involved in sleep and memory regulation (Tab. 2, Fig. 4, Ref. 59). Text in PDF www.elis.sk.

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“…These authors also showed a concomitant decrease in neuronal nitric oxide synthase (nNOS) protein levels. Khadrawy et al [41] on the other hand, showed that 72h of REM sleep deprivation increased hippocampal NO production without affecting cortical NO production. The neuronal phenotype within the hippocampus as well as the source of NO in our study remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…They further suggested that this alteration in the antioxidant defense system may account for the impaired maintenance of long term potentiation observed in these rats. Khadrawy et al [41] also reported that 72h of REM sleep deprivation increased lipid oxidation in both the hippocampus and the cortex. The levels of TBARS in the neocortex, brainstem and cerebellum were not altered in our study.…”

Section: Discussionmentioning

confidence: 99%

Sleep deprivation under sustained hypoxia protects against oxidative stress

Ramanathan

Siegel

2011

Free Radical Biology and Medicine

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We previously showed that total sleep deprivation increased antioxidant responses in several rat brain regions. We also reported that chronic hypoxia enhanced antioxidant responses and increased oxidative stress in rat cerebellum and pons, relative to normoxic conditions. In the current study, we examined the interaction between these two parameters (sleep and hypoxia). We exposed rats to total sleep deprivation under sustained hypoxia (SDSH), and compared changes in antioxidant responses and oxidative stress markers, in the neocortex, hippocampus, brainstem and cerebellum, to those in control animals left undisturbed under either sustained hypoxia (UCSH) or normoxia (UCN). We measured changes in total nitrite levels, as an indicator of nitric oxide (NO) production, superoxide dismutase (SOD) activity and total glutathione (GSHt) levels as markers of antioxidant responses and levels of thiobarbituric acid reactive substances (TBARS) and protein carbonyls as signs of lipid and protein oxidation products, respectively. We found that acute (6h) SDSH increased NO production in the hippocampus and increased GSHt levels in the neocortex, brainstem and cerebellum, while decreasing hippocampal lipid oxidation. Additionally, we observed increased hexokinase (HK) activity in the neocortex of SDSH rats compared to UCSH rats, suggesting that elevated glucose metabolism may be one potential source of the enhanced free radicals produced in this brain region. We conclude that short term insomnia under hypoxia may serve as an adaptive response to prevent oxidative stress.

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Effect of oxidative stress induced by paradoxical sleep deprivation on the activities of Na+, K+-ATPase and acetylcholinesterase in the cortex and hippocampus of rat

Cited by 42 publications

References 72 publications

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

Sleep Fragmentation Induces Cognitive Deficits Via Nicotinamide Adenine Dinucleotide Phosphate Oxidase–dependent Pathways in Mouse

The impact of sleep deprivation on hippocampal-mediated learning and memory in rats

Sleep deprivation under sustained hypoxia protects against oxidative stress

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