Altered aquaporins in the brains of mice submitted to intermittent hypoxia model of sleep apnea

Baronio, Diego; Martinez, Dênis; Fiori, Cíntia Zappe; Bambini-Júnior, Victorio; Forgiarini, Luiz Felipe; Rosa, Darlan Pase da; Kim, Lenise Jihe; Cerski, Marcelle Reesink

doi:10.1016/j.resp.2012.10.012

Cited by 43 publications

(30 citation statements)

References 27 publications

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“…Gadea et al (2008) demonstrated that the activation of endothelin-1 receptors in astrocytes promotes reactive astrogliosis after focal demyelination of corpus callosum. Our group previously demonstrated that 35 days of intermittent hypoxia induces reactive gliosis, astrocytes cell bodies hypertrophy, and neuronal damage in cerebellum, indicated by GFAP and S100B immunoreactivities (Baronio et al, 2013). Furthermore, endothelin-1 levels are also elevated in patients with multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (Haufschild et al, 2001).…”

Section: Bres : 43956mentioning

confidence: 96%

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Hypomyelination, memory impairment, and blood–brain barrier permeability in a model of sleep apnea

Kim¹,

Martinez²,

Fiori³

et al. 2015

Brain Research

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Section: Bres : 43956mentioning

confidence: 96%

“…In animal models utilizing exposure to intermittent hypoxia to simulate sleep apnea, neuronal deat Q6 h (Zhu et al, 2007) and neurocognitive dysfunctions were observed (Gozal et al, 2001). Our group previously described that cerebellum cells are more likely sensitive to intermittent hypoxia-induced lesions (Baronio et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Hypomyelination, memory impairment, and blood–brain barrier permeability in a model of sleep apnea

Kim¹,

Martinez²,

Fiori³

et al. 2015

Brain Research

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“…Mice were kept six each in cages measuring 30 x 19 x 13 cm, at an average room temperature of 22.4º ± 0.6° C and controlled humidity, on a standard 12/12 hour light-dark cycle (lights on at 0700, lights out at 1900). This method was described previously (18,19). All procedures were performed in accordance with the Guide for the Care and Use of Laboratory Animals (20) and were approved by the institutional animal care committee, Hospital de Clínicas de Porto Alegre (CEUA/HCPA #2009/09300).…”

Section: Animalsmentioning

confidence: 99%

“…The intermittent hypoxia procedure has been described previously in adult male mice (18,19), a mixture of 90% N 2 and 10% CO 2 was released into the cages over a period of 30 seconds, gradually reducing the oxy gen fraction to 7 ± 1% and increasing the CO 2 fraction to approximately 5 ± 1%; fans were then operated for 30 seconds so as to introduce room air into the cage. Overall, 480 such cycles of hypoxianormoxia occurred per day.…”

Section: Intermittent Hypoxia Systemmentioning

confidence: 99%

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Melatonin prevents hyperglycemia in a model of sleep apnea

Kaminski

Martinez

Fagundes

et al. 2015

Arch. Endocrinol. Metab.

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Objective: Obstructive sleep apnea is a common disorder associated with aging and obesity. Apneas cause repeated arousals, intermittent hypoxia, and oxidative stress. Changes in glucolipidic profile occur in apnea patients, independently of obesity. Animal models of sleep apnea induce hyperglycemia. This study aims to evaluate the effect of the antioxidants melatonin and N-acetylcysteine on glucose, triglyceride, and cholesterol levels in animals exposed to intermittent hypoxia. Materials and methods: Two groups of Balb/c mice were exposed to intermittent hypoxia (n = 36) or sham intermittent hypoxia (n = 36) for 35 days. The intermittent hypoxia group underwent a total of 480 cycles of 30 seconds reducing the inspired oxygen fraction from 21% to 7 ± 1% followed by 30 seconds of normoxia, during 8 hours daily. Melatonin or N-acetylcysteine were injected intraperitonially daily from day 21 on. Results: At day 35, glucose levels were significantly higher in the intermittent hypoxia group than in the control group. The intermittent hypoxia groups receiving N-acetylcysteine and vehicle showed higher glucose levels than the group receiving melatonin. The lipid profile was not affected by intermittent hypoxia or antioxidant administration. Conclusions:The present results suggest that melatonin prevents the well-recognized increase in glucose levels that usually follows exposure to intermittent hypoxia. Further exploration of the role of melatonin in sleep apnea is warranted. Arch Endocrinol Metab. 2015;59(1):66-70

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Effects of long-term treatment on brain volume in patients with obstructive sleep apnea syndrome

et al. 2015

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We assessed structural brain damage in obstructive sleep apnea syndrome (OSA) patients (21 males) and the effects of long-term continuous positive airway pressure (CPAP) treatment (18.2 ± 12.4 months; 8-44 months) on brain structures and investigated the relationship between severity of OSA and effects of treatment. Using deformation-based morphometry to measure local volume changes, we identified widespread neocortical and cerebellar atrophy in untreated patients compared to controls (59 males; Cohen's D = 0.6; FDR < 0.05). Analysis of longitudinally scanned magnetic resonance imaging (MRI) scans both before and after treatment showed increased brain volume following treatment (FDR < 0.05). Volume increase was correlated with longer treatment in the cortical areas that largely overlapped with the initial atrophy. The areas overlying the hippocampal dentate gyrus and the cerebellar dentate nucleus displayed a volume increase after treatment. Patients with very severe OSA (AHI > 64) presented with prefrontal atrophy and displayed an additional volume increase in this area following treatment. Higher impairment of working memory in patients prior to treatment correlated with prefrontal volume increase after treatment. The large overlap between the initial brain damage and the extent of recovery after treatment suggests partial recovery of non-permanent structural damage. Volume increases in the dentate gyrus and the dentate nucleus possibly likely indicate compensatory neurogenesis in response to diminishing oxidative stress. Such changes in other brain structures may explain gliosis, dendritic volume increase, or inflammation. This study provides neuroimaging evidence that revealed the positive effects of long-term CPAP treatment in patients with OSA.

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Altered aquaporins in the brains of mice submitted to intermittent hypoxia model of sleep apnea

Cited by 43 publications

References 27 publications

Hypomyelination, memory impairment, and blood–brain barrier permeability in a model of sleep apnea

Hypomyelination, memory impairment, and blood–brain barrier permeability in a model of sleep apnea

Melatonin prevents hyperglycemia in a model of sleep apnea

Effects of long-term treatment on brain volume in patients with obstructive sleep apnea syndrome

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