Navegando por Palavras-chave "paradoxical sleep deprivation"

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    Absence of oxidative stress following paradoxical sleep deprivation in rats
    (Elsevier B.V., 1997-10-10) DAlmeida, V; Hipolide, D. C.; Azzalis, L. A.; Lobo, L. L.; Junqueira, VBC; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    Paradoxical sleep deprivation was performed on rats using platform technique to investigate the oxidative process associated with it. Levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), total glutathione (GSH) and malondialdehyde production were measured in brain of rats under control conditions (C) and those on single large platforms (SLP), multiple large platforms (MLP), single small platforms (SSP) and multiple small platforms (MSP) groups. SOD, CAT and GPx brain activity and malondialdehyde production were not modified by any of the procedures. Brain GSH, however, was significantly reduced in both SSP and SLP groups. These results suggest that paradoxical sleep deprivation per se is not associated with oxidative damage. the observed alterations could be attributed to factors such as immobilization and social isolation present in the single platform techniques. (C) 1997 Elsevier Science Ireland Ltd.
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    Angiotensin I-converting enzyme (ACE) activity and expression in rat central nervous system after sleep deprivation
    (Walter de Gruyter & Co, 2011-04-01) Visniauskas, Bruna [UNIFESP]; Oliveira, Vitor [UNIFESP]; Carmona, Adriana K. [UNIFESP]; D'Almeida, Vania [UNIFESP]; Melo, Robson L. de; Tufik, Sergio [UNIFESP]; Chagas, Jair R. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Butantan Inst
    Proteases are essential either for the release of neuropeptides from active or inactive proteins or for their inactivation. Neuropeptides have a fundamental role in sleep-wake cycle regulation and their actions are also likely to be regulated by proteolytic processing. Using fluorescence resonance energy transfer substrates, specific protease inhibitors and real-time PCR we demonstrate changes in angiotensin I-converting enzyme (ACE) expression and proteolytic activity in the central nervous system in an animal model of paradoxical sleep deprivation during 96 h (PSD). Male rats were distributed into five groups (PSD, 24 h, 48 h and 96 h of sleep recovery after PSD and control). ACE activity and mRNA levels were measured in hypothalamus, hippocampus, brainstem, cerebral cortex and striatum tissue extracts. in the hypothalamus, the significant decrease in activity and mRNA levels, after PSD, was only totally reversed after 96 h of sleep recovery. in the brainstem and hippocampus, although significant, changes in mRNA do not parallel changes in ACE specific activity. Changes in ACE activity could affect angiotensin II generation, angiotensin 1-7, bradykinin and opioid peptides metabolism. ACE expression and activity modifications are likely related to some of the physiological changes (cardiovascular, stress, cognition, metabolism function, water and energy balance) observed during and after sleep deprivation.
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    Cardiovascular function alterations induced by acute paradoxical sleep deprivation in rats
    (Informa Healthcare, 2014-01-01) Almeida, F. R. [UNIFESP]; Perry, J. C. [UNIFESP]; Futuro-Neto, H. A.; Almeida, V. R. [UNIFESP]; Sebastiao, R. M. [UNIFESP]; Andersen, M. L. [UNIFESP]; Tufik, Sergio [UNIFESP]; Campos, R. R. [UNIFESP]; Bergamaschi, C. T. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Fed Espirito Santo; Fac Brasileira Med Sch
    Sleep loss has been implicated in triggering the hypertension. the goal of the present study was investigated the possible mechanisms underlying cardiovascular alterations after acute paradoxical sleep deprivation (PSD). Male Wistar rats were assigned in two experimental groups: (1) control and (2) PSD for 24 h using the modified single platform method. Paradoxical sleep deprived rats exhibited higher blood pressure, heart rate (HR) and impaired baroreceptor sensitivity. After pharmacological autonomic double blockade (propranolol and methylatropine administration), intrinsic heart rate was decreased after PSD. the PSD rats showed a reduction in the vagal tone without affecting sympathetic tone. Isoproterenol administration (0.001, 0.01 and 1 mu g/kg) induced an increase in Delta HR responses in PSD group. Electrocardiographic analysis in response to beta-adrenergic stimulation indicated that PSD contributed to ventricular cardiac arrhythmias. Our findings suggest that acute paradoxical sleep loss induce cardiovascular alterations, autonomic imbalance accompanied by impaired baroreflex sensitivity and increased arrhythmia susceptibility.
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    Cholinergic modulation of inhibitory avoidance impairment induced by paradoxical sleep deprivation
    (Elsevier B.V., 2000-05-01) Bueno, OFA; Oliveira, MGM; Lobo, L. L.; Morais, P. R.; Melo, FHM; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    1. Male Wister rats were submitted to paradoxical sleep deprivation for 96 hr by a modified multiple platform technique.2. Training of step-through inhibitory avoidance was performed immediately after the last day of paradoxical sleep deprivation. Twenty-four hr after training the animals were submitted to the retention test.3. in Experiment 1, pilocarpine (4 mg/kg, i.p.) or atropine (4 mg/kg, i.p.) were administered daily during. the paradoxical sleep deprivation period. Pilocarpine, but not atropine, reversed the impairment induced by PS deprivation.4. in Experiment 2, pilocarpine (4, 8 and 12 mg/kg, i.p.) was injected 1 hr before training in order to verify if the reversal of memory impairment was an effect secondary to residual enhanced blood levels of pilocarpine during training. Acute treatment with pilocarpine, in any dose, did not reverse the impairment produced by paradoxical sleep deprivation5. Activation of the cholinergic system during the period ol:deprivation is able to prevent memory deficits induced by paradoxical sleep deprivation.
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    Effects of paradoxical sleep deprivation on the performance of rats in a model of visual attention
    (Elsevier B.V., 2005-11-30) Godoi, FRD; Oliveira, MGM; Tufik, S.; Universidade Federal de São Paulo (UNIFESP)
    In the present work we sought to evaluate the effects of paradoxical sleep deprivation (PSD) on the performance of rats in the five-choice serial reaction time task, a test designed to assess attentional function. Adult male Wistar rats were trained to detect a brief (ls) light stimulus randomly presented in one of five locations in a box specially designed for the task. After achieving stable performance, the animals were submitted to 96 h of sleep deprivation by the platform technique, in which the rats are placed on top of small platforms in a tank filled with water. During sleep, particularly during the paradoxical stage, the loss of muscle tone make the animals fall into the water, thus awakening them and so depriving of sleep. Performance in the task was assessed daily during the 96 h deprivation period and also during seven recovery days afterwards. Paradoxical sleep deprivation reduced accuracy on the on the third (72 h) and fourth (96 h) days of sleep deprivation compared to home-cage controls, and this impairment reverted soon after the beginning of the recovery period. Sleep-deprived animals also showed an increase in omissions in the first day of PSD and a reduction on the number of trials started on the fourth day of sleep deprivation. No significant group differences were observed in premature and perseverative responses, correct response latency and reward latency. Our results thus indicate that paradoxical sleep deprivation impairs attentional function. (c) 2005 Elsevier B.V. All rights reserved.
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    Effects of pre- or post-training paradoxical sleep deprivation on two animal models of learning and memory in mice
    (Elsevier B.V., 2004-09-01) Silva, R. H.; Chehin, A. B.; Kameda, SR; Takatsu-Coleman, A. L.; Abilio, V. C.; Tufik, Sergio [UNIFESP]; Frussa, R.; Universidade Federal de São Paulo (UNIFESP)
    The aim of the present study was to verify the effects of pre- or post-training paradoxical sleep (PS) deprivation in mice tested in the passive and the plus-maze discriminative avoidance tasks. Three-month-old Swiss male mice were placed in narrow platforms in a water tank for 72 h to prevent the occurrence of PS. Control animals were kept in the same room, but in their home cages. Before or after this period, the animals were submitted to the training session of one of the behavioral tasks. the test sessions were performed 3 and 10 days after the training. the animals that were PS-deprived before the training session showed retention deficits in the test sessions performed 3 days later in both tasks (decreased latency to enter the dark chamber of the passive avoidance apparatus or increased percent time spent in the aversive arm of the plus-maze discriminative avoidance apparatus). Animals that were PS deprived after the training session showed no differences from control animals in the test sessions performed 3 days after the training in any of the tasks, but showed passive and discriminative avoidance retention deficits in the test performed 10 days after the training. the results suggest that both pre- and post-training paradoxical sleep deprivation produce memory deficits in mice. However, these effects have different temporal characteristics. (C) 2004 Elsevier Inc. All rights reserved.
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    Glucocorticoids are not responsible for paradoxical sleep deprivation-induced memory impairments
    (Amer Acad Sleep Medicine, 2008-04-01) Tiba, Paula Ayalko [UNIFESP]; Menezes Oliveira, Maria Gabriela [UNIFESP]; Rossi, Vanessa Contatto [UNIFESP]; Tufik, Sergio [UNIFESP]; Suchecki, Deborah [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Study Objectives: To evaluate whether paradoxical sleep deprivation-induced memory impairments are due to release of glucocorticoids, by means of corticosterone inhibition with metyrapone.Design: The design was a 2 (Groups [control, paradoxical sleep-deprived]) x 2 (Treatments [vehicle, metyrapone]) study, performed in 2 experiments: Acute treatment (single injection given immediately after 96 hours of sleep deprivation) and chronic treatment (8 injections, twice per day, throughout the sleep-deprivation period). Animals were either paradoxical sleep-deprived or remained in their home cages for 96 hours before training in contextual fear conditioning and received intraperitoneal injections of a corticosterone synthesis inhibitor, metyrapone. Memory performance was tested 24 hours after training.Subjects: Three-month old Wistar male rats.Measurements: Freezing behavior was considered as the conditioning index, and adrenocorticotropic hormone and corticosterone plasma levels were determined from trunk blood of animals sacrificed in different time points. Animals were weighed before and after the paradoxical sleep-deprivation period.Results: Acute metyrapone treatment impaired memory in control animals and did not prevent paradoxical sleep deprivation-induced memory impairment. Likewise, in the chronic treatment, paradoxical sleep-deprived animals did not differ from control rats in their corticosterone or adrenocorticotropic hormone response to training, but still did not learn as well, and did not show any stress responses to the testing. Chronic metyrapone was, however, effective in preventing the weight loss typically observed in paradoxical sleep-deprived animals.Conclusions: Our results suggest that glucocorticoids do not mediate memory impairments but might be responsible for the weight loss induced by paradoxical sleep deprivation.
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    Hormonal and behavioural responses of paradoxical sleep-deprived rats to the elevated plus maze
    (Blackwell Publishing Ltd, 2002-07-01) Suchecki, D.; Tiba, P. A.; Tufik, S.; Universidade Federal de São Paulo (UNIFESP)
    Activation of the hypothalamic-pituitary-adrenal (HPA) axis is observed immediately after 96 in of paradoxical sleep (PS) deprivation. However, when individually or group PS-deprived rats are challenged with a mild stressor, they exhibit a facilitation of the corticosterone response, and a faster return to basal levels than control rats. Because the housing condition influences coping behaviour, we tested whether the type of PS deprivation (individually or in group) influenced anxiety-like behaviour in the elevated plus-maze and the accompanying adrenocorticotropin (ACTH) and corticosterone responses. Individually (I-DEP) or group deprived (G-DEP) rats and their appropriate control groups were either killed immediately after 96 h of sleep deprivation (time-point 0 or 'basal') or exposed to a 5-min test on the elevated plus maze and sampled 5, 20 or 60 min after test onset. Control of I-DEP rats showed reduced locomotor activity and augmented anxiety-like behaviour, replicating the effects of social isolation. Although I-DEP rats exhibited higher motor activity than cage control rats, these groups did not differ in regard to the percentage of entry and time spent in the open arms. G-DEP rats, in turn, ambulated more, entered and remained longer in the open arms, exhibiting less anxiety-like behaviour. PS-deprived rats exhibited higher ACTH and corticosterone 'basal' secretion than control rats. for all groups, peak ACTH secretion was reached at the 5-min time-point, returning to unstressed basal levels 60 min after the test, except for G-DEP rats, which showed a return at 20 min. Peak levels of corticosterone occurred at 5 min for PS-deprived groups and at 20 min for control groups. G-DEP rats showed a return to 'basal' unstressed levels at 20 min, whereas the I-DEP and control groups did so at 60 min. A negative correlation between exploration in the open arms and hormone concentrations was observed. These data indicate that housing condition influences the subsequent behaviour of PS-deprived rats in the EPM which, in turn, seems to determine the secretion profile of ACTH and corticosterone in response to the test.
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    Increased ACTH and corticosterone secretion induced by different methods of paradoxical sleep deprivation
    (Blackwell Science Ltd, 1998-12-01) Suchecki, Deborah [UNIFESP]; Lobo, Leticia Leite [UNIFESP]; Hipólide, Débora Cristina [UNIFESP]; Tufik, Sergio [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The methods used to induce paradoxical sleep (PS) deprivation are believed to be stressful. in the present study, two methods were compared in regard to their ability to activate the hypothalamic-pituitary-adrenal (HPA) axis. Animals were placed on multiple large (MLP) or small (MSP) platforms or on single large (SLP) or small (SSP) platforms and blood sampled at the end of a 4-day period of PS deprivation (experiment 1) or on Days 1 (short-term) and 1 (long-term) of PS deprivation (experiment 2). ACTH and corticosterone (CORT) levels were determined by RIA. the results of experiment 1 showed that all experimental animals presented increased ACTH response, compared to controls. CORT levels, however, were only elevated in MSP animals, suggesting increased adrenal sensitivity. Experiment 2 showed that ACTH levels of MSP animals were higher than MLP and SSP animals, and that animals placed on the multiple platform tanks showed the highest ACTH levels on Day 4 of manipulation. CORT levels were elevated in the animals kept over small platforms. and these levels where higher on Day 1 than basal and further elevated on Day 4 of PS deprivation. These results indicate that the multiple platform technique induces a distinct activation of the I-IPA axis, and that PS deprivation may act as an additional stressor.
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    Palatable solutions during paradoxical sleep deprivation: Reduction of hypothalamic-pituitary-adrenal axis activity and lack of effect on energy imbalance
    (Blackwell Publishing Ltd, 2003-09-01) Suchecki, D.; Antunes, J.; Tufik, S.; Universidade Federal de São Paulo (UNIFESP)
    Paradoxical sleep deprivation (PSD) induces increased energy expenditure in rats, insofar as rats eat more but loose weight throughout the deprivation period. in the present study, rats were offered water, saccharin or sucrose to drink during the deprivation period, since it has been proposed that carbohydrates reduce the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Rats were submitted to the flower pot technique for 96 h. During the PSD period, they were weighed daily and food and fluid intake was assessed twice a day. At the end of the PSD period, rats were killed and plasma concentrations of glucose, adrenocorticotropic hormone (ACTH) and corticosterone were assayed. Compared to their control counterparts, all paradoxical sleep-deprived rats consumed more food, but lost weight. Paradoxical sleep-deprived rats given sucrose drank more than their control counterparts (especially in the light phase of the light/dark cycle). Paradoxical sleep-deprived rats showed increased food intake during all periods throughout the experiment, with peak intake during the dark phase and nadir during the light phase of the light/dark cycle. All paradoxical sleep-deprived rats showed lower glucose plasma levels than control rats and increased relative adrenal weight. However, when given saccharin or sucrose, paradoxical sleep-deprived rats showed lower concentrations of ACTH and corticosterone than their water-provided counterparts, indicating that palatable fluids were capable of lowering HPA axis activation produced by PSD. the fact that PSD induced energy imbalance regardless of the relative attenuation of the HPA axis activity produced by saccharin or sucrose suggests that the HPA axis may play only a secondary role in this phenomenon, and that other mechanisms may account for this effect. the data also suggest that supply of palatable fluids can be an additional modification to reduce the stress of the flower pot method.
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    Paradoxical sleep deprivation and sleep recovery: Effects on the hypothalamic-pituitary-adrenal axis activity, energy balance and body composition of rats
    (Blackwell Publishing, 2006-04-01) Hipolide, D. C.; Suchecki, D.; Pinto, APD; Faria, E. C.; Tufik, S.; Universidade Federal de São Paulo (UNIFESP); Univ Calif Riverside
    Numerous studies indicate that sleep deprivation alters energy expenditure. However, this conclusion is drawn from indirect measurements. in the present study, we investigated alterations of energy expenditure, body composition, blood glucose levels, plasma insulin, adrenocorticotropic hormone (ACTH) and corticosterone levels immediately after 4 days of sleep deprivation or after 4 days of sleep recovery. Rats were sleep deprived or maintained in a control environment (groups sleep-deprived/deprivation and control/deprivation). One half of these animals were sacrificed at the end of the deprivation period and the other half was transported to metabolic cages, where they were allowed to sleep freely (groups sleep-deprived/recovery and control/recovery). At the end of the sleep recovery period, these rats were sacrificed. After sleep deprivation, sleep-deprived rats exhibited loss of body weight, augmented energy expenditure and reduced metabolic efficiency compared to control rats. These alterations were normalised during the sleep recovery period. the body composition of sleep-deprived rats was altered insofar as there was a loss of fat content and gain of protein content in the carcass compared to control rats. However, these alterations were not reversed by sleep recovery. Finally, plasma levels of insulin were reduced during the sleep deprivation period in both control and sleep deprived groups compared to the recovery period. After the deprivation period, plasma ACTH and corticosterone levels were increased in sleep-deprived rats compared to control rats, and although ACTH levels were similar between the groups after the sleep recovery period, corticosterone levels remained elevated in sleep-deprived rats after this period. By means of direct measurements of metabolism, our results showed that sleep deprivation produces increased energy expenditure and loss of fat content. Most of the alterations were reversed by sleep recovery, except for corticosterone levels and body composition.
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    Paradoxical sleep deprivation facilitates subsequent corticosterone response to a mild stressor in rats
    (Elsevier B.V., 2002-03-01) Suchecki, D.; Tiba, P. A.; Tufik, S.; Universidade Federal de São Paulo (UNIFESP)
    The pituitary-ad renal responsiveness to a mild stressor was assessed in rats that were deprived of paradoxical sleep (PS) and in controls that were not deprived. Animals were either individually- or group-deprived for 96 h and hormone levels were assessed at 0, 5, 20 or 60 min after a saline injection + novelty and compared with rats which were not deprived. Both types of PS deprivation resulted in elevated adrenocorticotropin levels at 0 min, which peaked at 5 min in all animals. Individually-deprived rats exhibited the highest corticosterone (CORT) levels at 0 min. Peak levels were higher and occurred earlier in PS-deprived than in control rats (5 vs. 20 min, respectively). At 20 min, CORT levels had already returned to unstressed levels in PS-deprived rats, but not in control rats. These data indicate that PS deprivation induces facilitation of the adrenocortical response to a mild stressor, but do not suggest that PS deprivation changes the negative feedback sensitivity to CORT. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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    Paradoxical sleep deprivation induces muscle atrophy
    (Wiley-Blackwell, 2012-03-01) Dattilo, Murilo [UNIFESP]; Antunes, Hanna Karen Moreira [UNIFESP]; Medeiros, Alessandra [UNIFESP]; Mônico-Neto, Marcos [UNIFESP]; Souza, Helton de Sá; Lee, Kil Sun [UNIFESP]; Tufik, Sergio [UNIFESP]; Mello, Marco Tulio de [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); CEPE
    Introduction: Because paradoxical sleep deprivation (PSD) induces a catabolic hormone profile, we sought to evaluate the morphology of the tibialis anterior (TA) muscle and testosterone and corticosterone levels of paradoxical sleepdeprived rats.Methods: Three study groups of rats were established: the first group was sleep deprived for 96 h; the second group was also sleep deprived for 96 h, but then returned to their home-cage and allowed to sleep for the next 96 h; and the third group was the control group, with a normal sleep cycle. Results: PSD reduced the weight and fiber cross-sectional area of the TA muscle. Moreover, PSD enhanced plasma corticosterone and reduced serum testosterone levels. the 96 h of sleep after PSD was sufficient to restore partially the morphology of TA, while hormones returned to basal levels. Conclusion: PSD induces hormonal alterations that may mediate muscle atrophy. Muscle Nerve, 2012
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    Paradoxical Sleep Deprivation Modulates Tyrosine Hydroxylase Expression in the Nigrostriatal Pathway and Attenuates Motor Deficits Induced by Dopaminergic Depletion
    (Bentham Science Publ Ltd, 2012-06-01) Lima, Marcelo M. S.; Andersen, Monica Levy [UNIFESP]; Reksidler, Angela B.; Ferraz, Anete C.; Vital, Maria Aparecida Barbato Frazão [UNIFESP]; Tufik, Sergio [UNIFESP]; Univ Fed Parana; Universidade Federal de São Paulo (UNIFESP)
    The nigrostriatal pathway is very likely involved in sleep regulation, considering the occurrence and high prevalence of sleep-related disorders in patients with Parkinson's disease. Indeed, dopaminergic neurons in the ventral tegmental area were recently shown to fire in bursts during paradoxical sleep (PS), but little is known about the activity of the nigrostriatal dopamine (DA) cells in relation to PS. In view of that we hypothesized that paradoxical sleep deprivation (PSD) may play a relevant role in nigrostriatal tyrosine hydroxylase (TH) expression and, subsequently, in sleep rebound. The present study was designed to determine the effects of PSD in the nigrostriatal pathway in mice by means of neurochemical and behavioral approaches. Intraperitoneal reserpine (1 mg/kg) associated to alpha-methyl-p-tyrosine (MT) (250 mg/kg) to produce catecholamine depletion, or rotenone (10 mg/kg) to increase striatal DA turnover were injected 30 min before the 24 h of PSD. Catalepsy and open-field tests indicated that motor deficits induced by reserpine-MT were counteracted by PSD, which, in contrast, potentiated the motor impairment induced by rotenone. Besides, PSD produced down-regulation on TH expression within the substantia nigra pars compacta and striatum, without affecting the number or the optical density of dopaminergic neurons present in the respective areas. Interestingly, PSD potentiated the down-regulation of TH expression in the substantia nigra pars compacta and striatum induced by the co-administration of reserpine-MT. These results reinforce the notion of a strong participation of DA in PS, as a consequence of the modulation of TH protein expression in the nigrostriatal pathway..
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    Sleep rebound attenuates context-dependent behavioural sensitization induced by amphetamine
    (Elsevier B.V., 2008-07-01) Calzavara, Mariana Bendlin [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Fukushiro, Daniela Fukue [UNIFESP]; Lopez, Giorgia Batlle [UNIFESP]; Abilio, Vanessa Costhek [UNIFESP]; Tufik, Sergio [UNIFESP]; Frussa-Filho, Roberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    We have recently demonstrated that paradoxical sleep deprivation (PSD) potentiates the induction of amphetamine (AMPH)-induced behavioural sensitization by increasing its conditioned component. in the present study, the effects of sleep rebound (induced by 24 h recovery period from PSD) were studied on AMPH-induced behavioural sensitization. Sleep rebound attenuated the acute locomotor-stimulating effect of AMPH. AMPH-induced behavioural sensitization was context-specific and was also attenuated by sleep rebound. These results strengthen the notion that sleep conditions can influence AMPH-incluced behavioural sensitization. (C) 2008 Elsevier Inc. All rights reserved.