Effects of acute physical exercise in the light phase of sleep in rats with temporal lobe epilepsy.

OBJECTIVE: Our aim was to investigate the influence of an acute exercise session on sleep pattern in rats with temporal lobe epilepsy (TLE). METHODS: Twenty male Wistar rats were randomly assigned to 4 groups: control (C); acute exercise (EX); epilepsy (E) and epilepsy acute exercise (EEX). Two sleep electrocorticography recordings were performed during the light phase [baseline and day 2 (after the acute physical exercise session)]. After baseline recording, the exercise groups (EX and EEX) were submitted to an exercise session on a motor-driven treadmill at 12m/min for 30min. Twelve hours later, the rats were submitted to the second sleep recording. RESULTS: At baseline, the E group showed a higher wakefulness and a lower Total sleep time, Slow Wave Sleep and REM sleep compared with the C group. After acute exercise, there was an increase in Total sleep time and Slow Wave Sleep and a decrease of wakefulness in EEX (+11.10%, +20.29% and -11.25%, respectively) and EX (+5.20%, +11.60% and -8.12%, respectively) groups. CONCLUSION: These findings suggest that acute physical exercise positively impacts the sleep pattern of rats with TLE, inducing a more consolidated sleep.

Anxiety-like effects of meta-chlorophenylpiperazine in paradoxically sleep-deprived mice.

Chlorophenylpiperazines (CPP) are psychotropic drugs used in nightclub parties and are frequently used in a state of sleep deprivation, a condition which can potentiate the effects of psychoactive drugs. This study aimed to investigate the effects of sleep deprivation and sleep rebound (RB) on anxiety-like measures in mCPP-treated mice using the open field test. We first optimized our procedure by performing dose-effect curves and examining different pretreatment times in naïve male Swiss mice. Subsequently, a separate cohort of mice underwent paradoxical sleep deprivation (PSD) for 24 or 48h. In the last experiment, immediately after the 24h-PSD period, mice received an injection of saline or mCPP, but their general activity was quantified in the open field only after the RB period (24 or 48h). The dose of 5mgmL(-1) of mCPP was the most effective at decreasing rearing behavior, with peak effects 15min after injection. PSD decreased locomotion and rearing behaviors, thereby inhibiting a further impairment induced by mCPP. Plasma concentrations of mCPP were significantly higher in PSD 48h animals compared to the non-PSD control group. Twenty-four hours of RB combined with mCPP administration produced a slight reduction in locomotion. Our results show that mCPP was able to significantly change the behavior of naïve, PSD, and RB mice. When combined with sleep deprivation, there was a higher availability of drug in plasma levels. Taken together, our results suggest that sleep loss can enhance the behavioral effects of the potent psychoactive drug, mCPP, even after a period of rebound sleep.

The influence of sleep deprivation on expression of apoptosis regulatory proteins p53, bcl-2 and bax following rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide.

BACKGROUND: The aim of this study was to evaluate whether paradoxical sleep deprivation could affects the mechanisms and pathways essentials for cancer cells in tongue cancer induced by 4-nitroquinole 1-oxide in Wistar rats. MATERIALS AND METHODS: For this purpose, the animals were distributed into 4 groups of 5 animals each treated with 50 ppm 4 nitroquinoline 1 oxide (4 NQO) solution through their drinking water for 4 and 12 weeks. The animals were submitted to paradoxical sleep deprivation (PSD) for 72 h using the modified multiple platform method, which consisted of placing 5 mice in a cage (41 × 34 × 16 cm) containing 10 circular platforms (3.5 cm in diameter) with water 1 cm below the upper surface. The investigations were conducted using immunohistochemistry of p53, Bax and Bcl-2 proteins related to apoptosis and its pathways. Statistical analysis was performed by Kruskal-Wallis non-parametric test followed by the Dunn's test using SPSS software pack (version 1.0). P value < 0.05 was considered for statistic significance. RESULTS: Although no histopathological abnormalities were induced in the epithelium after 4 weeks of carcinogen exposure in all groups, in 12 weeks were observed pre-neoplasic lesions. Data analysis revealed statistically significant differences (P < 0.05) in 4 weeks group for p53 and for bcl-2 and for all immunomarkers after 12 weeks of 4NQO administration. CONCLUSION: Our results reveal that sleep deprivation exerted alterations in proteins associated with proliferation and apoptosis in carcinogenesis.

Influence of food restriction on lipid profile and spontaneous glucose levels in male rats subjected to paradoxical sleep deprivation.

OBJECTIVES: The purpose of this study was to determine the paired consequences of food restriction and paradoxical sleep deprivation on lipid profile and spontaneous glucose levels in male rats. METHOD: Food restriction began at weaning, with 6 g of food being provided per day, which was subsequently increased by 1 g per week until reaching 15 g per day by the eighth week. At adulthood, both rats subjected to food restriction and those fed ad libitum were exposed to paradoxical sleep deprivation for 96 h or were maintained in their home-cage groups. RESULTS: Animals subjected to food restriction exhibited a significant increase in high-density lipoprotein levels compared to animals that were given free access to food. After the paradoxical sleep deprivation period, the food-restricted animals demonstrated reduced concentrations of high-density lipoprotein relative to their respective controls, although the values for the food-restricted animals after sleep deprivation were still higher than those for the ad libitum group. The concentration of low-density lipoproteins was significantly increased in sleep-deprived animals fed the ad libitum diet. The levels of triglycerides, very low-density lipoproteins, and glucose in food-restricted animals were each decreased compared to both ad libitum groups. CONCLUSION: These results may help to illustrate the mechanisms underlying the relationship between sleep curtailment and metabolism and may suggest that, regardless of sleep deprivation, dietary restriction can minimize alterations in parameters related to cardiovascular risk.

Inhibition of self-grooming induced by sleep restriction in dam rats.

BACKGROUND & OBJECTIVES: Sleep restriction is a common feature of modern lifestyle and its effects can be extended to pregnancy. Several neurobehavioural consequences of sleep restriction during pregnancy have been reported, among which stand out perinatal depression and maternal fatigue, however, its effects over mother-infant relationship warrant further investigation. Thus, this study was aimed to evaluate the effects of sleep restriction during pregnancy over maternal behaviour and maternal aggression through animal models. METHODS: Eighteen 90-day-old female Wistar rats were distributed in two groups: (i) Control - not submitted to any manipulation during pregnancy, and (ii) Sleep restriction - submitted to sleep restriction during the entire pregnancy (21 days) through the multiple platforms technique. In the postpartum day 5, resident-intruder paradigm and the latencies test were performed to assess both maternal behaviour and maternal aggression. RESULTS: The sleep-restricted females displayed grooming in less frequency and duration, and with higher latency when compared to normal animals, while maternal aggression and maternal behaviour parameters remained equivalent between groups. INTERPRETATION & CONCLUSIONS: Considering the maintenance of maternal behavioural parameters, the inhibition of grooming seems to exert an adaptive mechanism, enabling sleep-restricted rats to display maternal behaviour properly.

Influence of food restriction on lipid profile and spontaneous glucose levels in male rats subjected to paradoxical sleep deprivation

OBJECTIVES: The purpose of this study was to determine the paired consequences of food restriction and paradoxical sleep deprivation on lipid profile and spontaneous glucose levels in male rats. METHOD: Food restriction began at weaning, with 6 g of food being provided per day, which was subsequently increased by 1 g per week until reaching 15 g per day by the eighth week. At adulthood, both rats subjected to food restriction and those fed ad libitum were exposed to paradoxical sleep deprivation for 96 h or were maintained in their home-cage groups. RESULTS: Animals subjected to food restriction exhibited a significant increase in high-density lipoprotein levels compared to animals that were given free access to food. After the paradoxical sleep deprivation period, the foodrestricted animals demonstrated reduced concentrations of high-density lipoprotein relative to their respective controls, although the values for the food-restricted animals after sleep deprivation were still higher than those for the ad libitum group. The concentration of low-density lipoproteins was significantly increased in sleep-deprived animals fed the ad libitum diet. The levels of triglycerides, very low-density lipoproteins, and glucose in foodrestricted animals were each decreased compared to both ad libitum groups. CONCLUSION: These results may help to illustrate the mechanisms underlying the relationship between sleep curtailment and metabolism and may suggest that, regardless of sleep deprivation, dietary restriction can minimize alterations in parameters related to cardiovascular risk.

Sleep loss induces differential response related to genotoxicity in multiple organs of three different mice strains.

The purpose of the present study was to determine the genetic damage induced by paradoxical sleep deprivation (PSD) in three different male mice strains in peripheral blood, heart, kidney and liver tissues by the single cell gel (comet) assay. Swiss, C57BL/6j and hairless (HRS/j) mice were submitted to PSD by the multiple platform technique for 72 hr, and DNA damage was evaluated. Statistically significant differences in DNA damage were found in blood cells of the Swiss mice strain when compared to negative controls. By contrast, no statistically significant differences were found in the C57BL/6j or hairless mice strains. With regard to the liver, extensive genotoxic effects were found in the Swiss strain. The hairless and C57BL/6j mice strains did not show any signs of genotoxocity in this organ. The same lack of effect was noted in kidney and heart cells of all strains evaluated. In conclusion, our results reveal that sleep deprivation exerted genetic damage in the form of DNA breakage in blood and liver cells of the Swiss mice strain only. This type of approach should be considered when studying noxious activities on genetic apparatus induced by sleep deprivation in mice since the Swiss strain is more suitable for this purpose.