Navegando por Palavras-chave "Rebound"

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    Age-related changes during a paradigm of chronic sleep restriction
    (Elsevier B.V., 2010-12-10) Souza, Luciane de [UNIFESP]; Andersen, Monica L. [UNIFESP]; Smaili, Soraya Soubhi [UNIFESP]; Lopes, Guiomar S. [UNIFESP]; Ho, Priscila S. [UNIFESP]; Papale, Ligia A. [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Fragmented and restricted sleep is a common problem for the human elderly. There is evidence that aging impairs sleep in animals as well. After sleep deprivation, older animals have less sleep rebound. Despite increasing complaints of reduced time for sleep in contemporary society, few studies have examined chronic sleep restriction protocols in animals. Therefore, the aim of the present study was to evaluate the effects of chronic sleep restriction on the sleep patterns of aged rats. Using the single platform method, 22-month-old male rats were submitted to 18 h of sleep restriction followed by 6 h of total sleep opportunity. the sleep-wake cycles of these rats were recorded for 6 h/day throughout the 12-day procedure. the results showed that total sleep time and NREM sleep were reduced during the 12-day sleep restriction period. However, rebound REM sleep was only significant on day 6. A negative rebound was also seen, particularly during the last days of the chronic sleep restriction period. Furthermore, sleep latency and mean wake bout length progressively increased during the protocol. These findings indicate that older rats have an inability to restore their sleep patterns during extended sleep deprivation. (C) 2010 Elsevier B.V. All rights reserved.
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    Distinct effects of acute and chronic sleep loss on DNA damage in rats
    (Elsevier B.V., 2009-04-30) Andersen, Monica Levy [UNIFESP]; Ribeiro, Daniel Araki [UNIFESP]; Bergamaschi, Cassia Toledo [UNIFESP]; Alvarenga, Tathiana Aparecida [UNIFESP]; Silva, Andressa [UNIFESP]; Zager, Adriano [UNIFESP]; Campos, Ruy Ribeiro [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The aim of this investigation was to evaluate genetic damage induced in male rats by experimental sleep loss for short-term (24 and 96 h) and long-term (21 days) intervals, as well as their respective recovery periods in peripheral blood, brain, liver and heart tissue by the single cell gel (comet) assay. Rats were paradoxically deprived of sleep (PSD) by the platform technique for 24 or 96 h, or chronically sleep-restricted (SR) for 21 days. We also sought to verify the time course of their recovery after 24 h of rebound sleep. the results showed DNA damage in blood cells of rats submitted to PSD for 96 h. Brain tissue showed extensive genotoxic damage in PSD rats (both 24 and 96 h), though the effect was more pronounced in the 96 h group. Rats allowed to recover from the PSD-96 h and SR-21 days treatments showed DNA damage as compared to negative controls. Liver and heart did not display any genotoxicity activity. Corticosterone concentrations were increased after PSD (24 and 96 h) relative to control rats, whereas these levels were unaffected in the SR group. Collectively, these findings reveal that sleep loss was able to induce genetic damage in blood and brain cells, especially following acute exposure. Since DNA damage is an important step in events leading to genomic instability, this study represents a relevant contribution to the understanding of the potential health risks associated with sleep deprivation. (C) 2009 Elsevier Inc. All rights reserved.
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    Effects of cocaine, methamphetamine and modafinil challenge on sleep rebound after paradoxical sleep deprivation in rats
    (Associação Brasileira de Divulgação Científica, 2008-01-01) Martins, Raquel Cristina Silva [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Shih, Ming Chi [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Sleep loss is both common and critically relevant to our society and might lead to the abuse of psychostimulants such as amphetamines, cocaine and modafinil. Since psychoactive substance abuse often occurs within a scenario of sleep deficit, the purpose of this investigation was to compare the sleep patterns of rats challenged with cocaine (7 mg/kg, ip), methamphetamine (7 mg/kg, ip), or modafinil (100 mg/kg, ip) subsequent to paradoxical sleep deprivation (PSD) for 96 h. Our results show that, immediately after 96 h of PSD, rats (10 per group) that were injected with a psychostimulant presented lower percentages of paradoxical sleep compared to those injected with saline (P < 0.01). Regarding slow wave sleep (SWS), rats injected with psychostimulants after PSD presented a late rebound (on the second night subsequent to the injection) in the percentage of this phase of sleep when compared to PSD rats injected with saline (P < 0.05). In addition, the current study has produced evidence of the characteristic effect of each drug on sleep architecture. Home cage control rats injected with modafinil and methamphetamine showed a reduction in SWS compared with the saline group. Methamphetamine affected sleep patterns most, since it significantly reduced paradoxical sleep, SWS and sleep efficiency before and after PSD compared to control (P < 0.05). Cocaine was the psychostimulant causing the least changes in sleep pattern in relation to those observed after saline injection. Therefore, our results suggest that abuse of these psychostimulants in a PSD paradigm aggravates their impact on sleep patterns.
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    Impairment of the mitochondrial electron transport chain due to sleep deprivation in mice
    (Elsevier B.V., 2010-09-01) Andreazza, Ana C.; Andersen, Monica L. [UNIFESP]; Alvarenga, Tathiana A. [UNIFESP]; de-Oliveira, Marcos R.; Armani, Fernanda [UNIFESP]; Ruiz, Francieli S. [UNIFESP]; Giglio, Larriany; Moreira, Jose C. F.; Kapczinski, Flavio; Tufik, Sergio [UNIFESP]; Univ Fed Rio Grande do Sul; Univ British Columbia; Universidade Federal de São Paulo (UNIFESP)
    It has been demonstrated that sleep deprivation is associated with altered expression of genes related to metabolic processes, response to stress and inflammation, circadian sleep/wake cycles, regulation of cell proliferation and various signaling pathways. However, the molecular mechanisms underlying these changes remain poorly understood. Thus, the present study aims to characterize the function of the mitochondrial electron transport chain in the brain using an animal model of paradoxical sleep deprivation (PSD). the question of whether sleep recovery (rebound) can reverse changes found after PSD is also addressed. Adult male inbred C57BL/6 J mice were randomly distributed into three groups: home-cage control, PSD and sleep rebound groups. the PSD and rebound groups were subjected to PSD for 72 h. After this sleep deprivation period, the rebound group was returned to its home cage and allowed to sleep in an undisturbed and spontaneous fashion for 24 h. the mitochondrial complex complex II, succinate dehydrogenase and complex II-III activities were then measured by spectrophotometric methods in sub-mitochondrial particles extracted from the prefrontal cortex, hippocampus, striatum and hypothalamus. Our results showed a significant decrease in the activity of complex in the PSD and rebound groups as compared to the control group. the complex II and II-III activity were particularly decreased in the hypothalamus of the sleep rebound group. These results are consistent with the involvement of sleep in energy metabolism and corroborate previous experiments demonstrating the importance of the hypothalamus in sleep regulation. (C) 2010 Elsevier B.V. All rights reserved.
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    Increased susceptibility to development of anhedonia in rats with chronic peripheral nerve injury: Involvement of sleep deprivation?
    (Elsevier B.V., 2009-08-31) Andersen, Monica L. [UNIFESP]; Hoshino, Katsumasa; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual Paulista
    The Main purpose of the present study was to evaluate whether REM sleep deprivation (RSD) influences the development of anhedonia in rats in a peripheral neuropathy model induced by sciatic nerve constriction injury (CCI). Anhedonia was measured by assessing daily water/sucrose intake. Four groups were assessed: control (CTRL), CCI, RSD, and CCI + RSD (n = 8/group). Intake data were collected at baseline (mean of 3 days), on the 1st and 2nd days after a CCI or SHAM procedure, during 4 days of RSD, and during an additional 10 days (rebound period or equivalent in home-cage rats). Control rats spontaneously and progressively increased Sucrose intake, reaching final daily volumes significantly greater than respective initial baseline amounts. RSD promoted an additional and immediate significant increase in sucrose intake during sleep deprivation days. the CCI group did not display a spontaneous, progressive increase in sucrose intake. When CO was combined with RSD, the increase in sucrose intake induced by RSD was significantly lower than in animals submitted to RSD alone; the (CCI + RSD) group also failed to show a spontaneous and progressive increase in sucrose intake. the present findings indicate that animal model of chronic neuropathy exhibits reduced sucrose ingestion. Accordingly, this anhedonic condition that constitutes to the core manifestation of depressive states did not occur in response to a single episode of total RSD. (C) 2009 Elsevier Inc. All rights reserved.
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    Paradoxical sleep deprivation impairs acquisition, consolidation, and retrieval of a discriminative avoidance task in rats
    (Elsevier B.V., 2008-11-01) Alvarenga, Tathiana A. [UNIFESP]; Patti, Camilla L. [UNIFESP]; Andersen, Monica L. [UNIFESP]; Silva, Regina H.; Calzavara, Mariana B. [UNIFESP]; Lopez, Giorgia B. [UNIFESP]; Frussa-Filho, Roberto [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Fed Rio Grande do Norte
    The aim of the present study was to investigate the effects of paradoxical sleep deprivation (PSD) for 96 h on the learning/memory processes in rats submitted to the plus-maze discriminative avoidance task (PMDAT). which simultaneously evaluates learning. memory, anxiety and motor function. Four experiments were performed in which rats were submitted to: (1) post-training and pre-test PSD; (2) post-training or pre-test PSD: (3) pre-training PSD or pre-training paradoxical sleep (PS) rebound (24 h) and (4) pre-test PSD rebound. Concerning Experiment 1, post-training and pre-test PSD induced memory deficits, an anxiolytic-like behavior and an increase in locomotor activity. in Experiment II, both post-training PS-deprived and pre-test PS-deprived groups showed memory deficits per se. However, only the pre-test PS-deprived animals presented anxiolytic-like behavior and increased locomotor activity. in Experiment III, pre-training PS-deprived rats showed learning and memory deficits, anxiolytic-like behavior and increased locomotor activity. A 24 h-sleep recovery period after the PSD abolished the learning and memory deficits but not anxiety and locomotor alterations. Finally, sleep rebound did not modify acquisition (Experiment III) and retrieval (Experiment IV). This study strengthened the critical role of paradoxical sleep (but not sleep rebound) in all the phases of learning and memory formation. in addition, it suggests that PSD effects on acquisition and consolidation do not seem to be related to other behavioral alterations induced by this procedure. (C) 2008 Elsevier Inc. All rights reserved.
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    Paradoxical sleep deprivation impairs mouse survival after infection with malaria parasites
    (Biomed Central Ltd, 2015-04-28) Lungato, Lisandro [UNIFESP]; Gazarini, Marcos Leoni [UNIFESP]; Paredes-Gamero, Edgar Julian [UNIFESP]; Tufik, Sergio [UNIFESP]; D'Almeida, Vania [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Background: Parasitic diseases like malaria are a major public health problem in many countries and disrupted sleep patterns are an increasingly common part of modern life. the aim of this study was to assess the effects of paradoxical sleep deprivation (PSD) and sleep rebound (RB) on malarial parasite infection in mice.Methods: After PSD, one group was immediately infected with parasites (PSD). the two other PSD rebound groups were allowed to sleep normally for either 24 h (24 h RB) or 48 h (48 h RB). After the recovery periods, mice were inoculated with parasites.Results: the PSD group was the most affected by parasites presenting the higher death rate (0.02), higher number of infected cells (p < 0.01), and decrease in body weight (p < 0.04) compared to control and 48 h RB groups. the 24 h RB group was also different from control group in survival (p < 0.03), number of infected cells (p < 0.05) and body weight (p < 0.04). After 48 hours of sleep rebound animals were allowed to restore their response to parasitic infection similar to normal sleep animals.Conclusions: These results suggest that PSD is damaging to the immune system and leads to an increased infection severity of malaria parasites; only 48 hours of recovery sleep was sufficient to return the mice infection response to baseline values.