Highlights of PiezoSleep System From Recent Literature
Drug induced alterations in sleep patterns identified with the PiezoSleep system.
Researchers at the University of Texas investigated circadian and sleep altering effects of two drugs used to treat conditions with known circadian components; Verapamil is used to treat cluster headaches, which occur at roughly the same time of day for most patients, and Moricizine was previously used to treat arrhythmia, where cardiac events are known to occur more frequently in the morning.
Following identification of circadian effects of the drugs in vitro, the investigators used the PiezoSleepTM system to assess drug related changes in sleep patterns in mice, identifying alterations in the time of sleep onset, sleep bout-lengths, and in light vs dark period sleep. Verapamil, a calcium channel blocker used to treat cluster headaches, migraines, hypertension, and angina, altered the time of sleep, but not total sleep, in a sex specific manner in mice. Male mice treated with verapamil slept more in the light period; treated female mice slept more in the dark (active) period, with shorter average sleep bout durations. Verapamil reduced activity levels in both sexes, and reduced the free running period both in vitro and in vivo. In a separate study, Moricizine was found to increase the total amount of sleep in mice, particularly in the early dark period, when mice are usually most active. In vitro, Moricizine was found to lengthen the circadian cycle in a dose dependent manner.
These studies highlight the utility of the PiezoSleepTM system for efficiently investigating drug induced changes in sleep patterns without the need for surgery and EEG monitoring, facilitating higher powered studies with larger number of animals in drug screening studies, at lower cost.
The PiezoSleep system is used to evaluate SARM1 as a target for intervention in Traumatic Brain Injury
Sleep disruption is a common comorbidity of traumatic brain injury (TBI), chronically affecting approximately half of individuals who have had a mild, moderate or severe traumatic brain injury. Researchers at Uniformed Services University included the PiezoSleepTM system in a study to assess the potential of SARM1 (sterile alpha and Toll/interleukin-1 receptor motif-containing 1) as a target for therapeutic intervention following TBI. SARM1 initiates a programmed pathway that depletes energy stores and results in structural breakdown of axons following injury.
In this model of chronic TBI, atrophy of the corpus collosum, and behavior tests including sleep, were compared in TBI vs sham injured wild type (WT) and SAMR1 knock-out (KO) mice. Longitudinal MRI volumetric measurements of the corpus collosum in mice following TBI at 3 days (acute injury) and ten weeks (chronic stage), compared to baseline (pre-injury) measurements showed a higher level of atrophy in WT mice compared to SARM1 KO mice at ten weeks post-injury. In agreement with this observation, axons of SARM1 KO mice had less damage than axons of WT mice at ten weeks post-injury by multiple histological measures. Sleep studies at eight weeks post-injury identified reduced sleep in WT TBI mice compared to sham treated WT mice, whereas there was no statistical difference in percent sleep between TBI and sham treated SARM1 KO mice. Disrupted sleep in WT TBI mice occurred during the light period, or subjective night, for mice. Collectively, these results provide evidence for preservation of axon integrity and function following TBI when SARM1 is disabled, indicating SARM1 as a viable target for therapeutic intervention. Sleep monitoring indicates that sleep disruption is present in this chronic TBI mouse model, and may be a useful in vivo indicator of progressive disease. Sleep monitoring post-TBI over multiple weeks would be useful to identify when sleep disruption first appears and whether it continues, worsens, or changes over time. Noninvasive sleep tracking with PiezoSleepTM is ideal for longitudinal data collection in TBI models, where mice have already experienced brain trauma, with the added benefit of lower cost and automated data collection in multiple groups of mice.
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Mechanisms of homeostatic regulation of GABA type A receptors by accessory protein Shisa7, with observed differences in tonic inhibition in sleep and wake.
Researchers at the National Institute of Health investigated the role of Shisa7 in modulating tonic inhibition in the hippocampus using cultured hippocampal CA1 neurons, mouse hippocampal slices, and by comparing tonic current in sleep and wake states in Shisa7 Knockout (KO) and wild-type (WT) mice.
The results from this study provide evidence that PKA phosphorylation of Shisa7 promotes exocytosis of α5-GABAAR, thereby increasing tonic inhibition in the hippocampus via increased levels of α5-GABAAR at the extrasynaptic neuronal surface. Differences in tonic inhibition mediated by Shisa7 in sleep and wake states were investigated by measuring tonic current in hippocampal slices from WT and Shisa7 Knockout KO mice that had been in extended sleep or wake states (4 hours), monitored by the PiezoSleepTM system, at the time of sacrifice. Tonic current was found to be higher during wake than in sleep, and modulated by Shisa7, as observed by sleep vs wake differences in WT mice that were not present in Shisa7 KO mice.
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