Isoflurane anesthesia and sleep deprivation trigger delayed and selective sleep alterations.

Isoflurane anesthesia (IA) partially compensates NREM sleep (NREMS) and not REM sleep (REMS) requirement, eliciting post-anesthetic REMS rebound. Sleep deprivation triggers compensatory NREMS rebounds and REMS rebounds during recovery sleep as a result of the body's homeostatic mechanisms. A combination of sleep deprivation and isoflurane anesthesia is common in clinical settings, especially prior to surgeries. This study investigates the effects of pre-anesthetic sleep deprivation on post-anesthetic sleep-wake architecture. The effects of isoflurane exposure (90 min) alone were compared with the effects of isoflurane exposure preceded by experimental sleep deprivation (6 h, gentle handling) on recovery sleep in adult mice by studying the architecture of post-anesthetic sleep for 3 consecutive post-anesthetic days. Effects of isoflurane anesthesia on recovery sleep developed only during the first dark period after anesthesia, the active phase in mice. During this time, mice irrespective of preceding sleep pressure, showed NREMS and REMS rebound and decreased wakefulness during recovery sleep. Additionally, sleep deprivation prior to isoflurane treatment caused a persistent reduction of theta power during post-anesthetic REMS at least for 3 post-anesthetic days. We showed that isoflurane causes NREMS rebound during recovery sleep which suggests that isoflurane may not fully compensate for natural NREMS. The study also reveals that isoflurane exposure preceded by sleep deprivation caused a persistent disruption of REMS quality. We suggest that preoperative sleep deprivation may impair postoperative recovery through lasting disruption in sleep quality.

Crosstalk between the subiculum and sleep-wake regulation: A review.

The circuitry underlying the initiation, maintenance, and coordination of wakefulness, rapid eye movement sleep, and non-rapid eye movement sleep is not thoroughly understood. Sleep is thought to arise due to decreased activity in the ascending reticular arousal system, which originates in the brainstem and awakens the thalamus and cortex during wakefulness. Despite the conventional association of sleep-wake states with hippocampal rhythms, the mutual influence of the hippocampal formation in regulating vigilance states has been largely neglected. Here, we focus on the subiculum, the main output region of the hippocampal formation. The subiculum, particulary the ventral part, sends extensive monosynaptic projections to crucial regions implicated in sleep-wake regulation, including the thalamus, lateral hypothalamus, tuberomammillary nucleus, basal forebrain, ventrolateral preoptic nucleus, ventrolateral tegmental area, and suprachiasmatic nucleus. Additionally, second-order projections from the subiculum are received by the laterodorsal tegmental nucleus, locus coeruleus, and median raphe nucleus, suggesting the potential involvement of the subiculum in the regulation of the sleep-wake cycle. We also discuss alterations in the subiculum observed in individuals with sleep disorders and in sleep-deprived mice, underscoring the significance of investigating neuronal communication between the subiculum and pathways promoting both sleep and wakefulness.

Electroencephalographic monitoring of anesthesia during surgical procedures in mice using a modified clinical monitoring system.

Monitoring brain activity and associated physiology during the administration of general anesthesia (GA) in mice is pivotal to guarantee postanesthetic health. Clinically, electroencephalogram (EEG) monitoring is a well-established method to guide GA. There are no established methods available for monitoring EEG in mice (Mus musculus) during surgery. In this study, a minimally invasive rodent intraoperative EEG monitoring system was implemented using subdermal needle electrodes and a modified EEG-based commercial patient monitor. EEG recordings were acquired at three different isoflurane concentrations revealing that surgical concentrations of isoflurane anesthesia predominantly contained burst suppression patterns in mice. EEG suppression ratios and suppression durations showed strong positive correlations with the isoflurane concentrations. The electroencephalographic indices provided by the monitor did not support online monitoring of the anesthetic status. The online available suppression duration in the raw EEG signals during isoflurane anesthesia is a straight forward and reliable marker to assure safe, adequate and reproducible anesthesia protocols.

Discriminating rapid eye movement sleep from wakefulness by analyzing high frequencies from single-channel EEG recordings in mice.

Rapid eye movement sleep (REMS) is characterized by the appearance of fast, desynchronized rhythms in the cortical electroencephalogram (EEG), similar to wakefulness. The low electromyogram (EMG) amplitude during REMS distinguishes it from wakefulness; therefore, recording EMG signal seems to be imperative for discriminating between the two states. The present study evaluated the high frequency components of the EEG signal from mice (80-500 Hz) to support REMS detection during sleep scoring without an EMG signal and found a strong positive correlation between waking and the average power of 80-120 Hz, 120-200 Hz, 200-350 Hz and 350-500 Hz. A highly negative correlation was observed with REMS. Furthermore, our machine learning approach demonstrated that simple EEG time-series features are enough to discriminate REMS from wakefulness with sensitivity of roughly 98 percent and specificity of around 92 percent. Interestingly, assessing only the higher frequency bands (200-350 Hz as well as 350-500 Hz) gives significantly greater predictive power than assessing only the lower end of the EEG frequency spectrum. This paper proposes an approach that can detect subtle changes in REMS reliably, and future unsupervised sleep-scoring approaches could greatly benefit from it.