After the rats were offered 0 1% sodium saccharin (Sac) as condit

After the rats were offered 0.1% sodium saccharin (Sac) as conditioned stimulus (CS), an intra peritoneal (i.p.) injection of several concentrations (5-30 mg/kg) of midazolam was followed by an i.p. injection of 0.15 M LiCl (2% of body weight) as unconditioned

stimulus (US). The rats, which acquired CTA by every CS-US paradigm, strongly avoided Sac on the 1st test day after conditioning and maintained the avoidance for 3 days. We have already reported that Sac intake abruptly increased on the 2nd test day and the almost complete extinction occurred on the 3rd click here test day after conditioning by injection of subhypnotic dose of propofol before LiCl-injection. In contrast, we found that subhypnotic dose of midazolam suppressed not only CTA acquisition, but also CTA retention. On the other hand, an alpha 2-adrenergic blocker, yohimbin (1 mg/kg) suppressed only the CIA retention. These results suggest that the subhypnotic doses of midazolam firstly affect the acquisition mechanism of the GSK3326595 in vivo CTA memory (CTAM), resulting the suppression of the retention of CTAM. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“A physiologically based quantitative

model of the human ascending arousal system is used to study sleep deprivation after being calibrated on a small set of experimentally based criteria. The model includes the sleep-wake switch of mutual inhibition between nuclei which use monoaminergic neuromodulators, and the ventrolateral preoptic area. The system is driven by the circadian rhythm and sleep homeostasis. We use a small number of experimentally derived criteria to calibrate the model for sleep deprivation, then investigate model predictions for other experiments, demonstrating the scope of application. Daporinad in vitro Calibration gives an improved parameter set, in which the form of the homeostatic drive is better constrained, and its weighting relative to the circadian drive is increased. Within the newly constrained parameter ranges, the model predicts

repayment of sleep debt consistent with experiment in both quantity and distribution, asymptoting to a maximum repayment for very long deprivations. Recovery is found to depend on circadian phase, and the model predicts that it is most efficient to recover during normal sleeping phases of the circadian cycle, in terms of the amount of recovery sleep required. The form of the homeostatic drive suggests that periods of wake during recovery from sleep deprivation are phases of relative recovery, in the sense that the homeostatic drive continues to converge toward baseline levels. This undermines the concept of sleep debt, and is in agreement with experimentally restricted recovery protocols. Finally, we compare our model to the two-process model, and demonstrate the power of physiologically based modeling by correctly predicting sleep latency times following deprivation from experimental data. (C) 2008 Elsevier Ltd.

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