Behavioural brain research
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Comparative Study
Sleep homeostasis in rats assessed by a long-term intermittent paradoxical sleep deprivation protocol.
Numerous studies have evaluated the sleep homeostasis of rats after short- or long-periods of sleep deprivation, but none has assessed the effects of prolonged sleep restriction on the rat's sleep pattern. The purpose of the present study, therefore, was to evaluate the sleep homeostasis of rats under a protocol of chronic sleep restriction. Male Wistar rats were implanted with electrodes for EEG and EMG recordings. ⋯ High amplitude slow wave sleep was also greatly affected by the protocol. Nonetheless, one day of recovery was sufficient to restore the normal sleep pattern. These findings indicate that this protocol was capable to induce many changes in the rat's sleep patterns, suggesting that during the 6h sleep window there is a sleep adaptive homeostatic process.
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Comparative Study
Secondary hypoxia exacerbates acute disruptions of energy metabolism in rats resulting from fluid percussion injury.
The purpose of these experiments was to determine whether secondary hypoxia exacerbates the metabolic consequences of fluid percussion injury (FPI). In Experiment I, rats were trained to press a lever for their entire daily ration of food at any time during a 12-h light/dark cycle and run in an activity wheel. After food intake and body weight stabilized, rats were surgically prepared, assigned to one of four groups [FPI+Hypoxia (IH), FPI+Normoxia (IN), Sham Injury+Hypoxia (SH), Sham Injury+Normoxia (SN)] and, after recovery from surgery, anesthetized with halothane delivered by a 21% O2 source. ⋯ Immediately after 30 min of hypoxia or normoxia, rats were confined to metabolism cages that were used to quantify rates of oxygen consumption (VO2), carbon dioxide production (VCO2), and heat production (H). Post-traumatic hypoxia exacerbated the FPI-induced increases in VO2, VCO2, and H. The results of Experiments I and II provide convergent confirmation that secondary hypoxemia exacerbates the FPI-induced hypermetabolic state in rats and therefore might significantly exacerbate the brain injury-induced disruptions of energy metabolism in humans.