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Dynamic- and Frequency-Specific Regulation of Sleep Oscillations by Cortical Potassium Channels


Muheim, Christine M; Spinnler, Andrea; Sartorius, Tina; Dürr, Roland; Huber, Reto; Kabagema, Clement; Ruth, Peter; Brown, Steven A (2019). Dynamic- and Frequency-Specific Regulation of Sleep Oscillations by Cortical Potassium Channels. Current Biology, 29(18):2983-2992.e3.

Abstract

Primary electroencephalographic (EEG) features of sleep arise in part from thalamocortical neural assemblies, and cortical potassium channels have long been thought to play a critical role. We have exploited the regionally dynamic nature of sleep EEG to develop a novel screening strategy and used it to conduct an adeno-associated virus (AAV)-mediated RNAi screen for cellular roles of 31 different voltage-gated potassium channels in modulating cortical EEG features across the circadian sleep-wake cycle. Surprisingly, a majority of channels modified only electroencephalographic frequency bands characteristic of sleep, sometimes diurnally or even in specific vigilance states. Confirming our screen for one channel, we show that depletion of the KCa1.1 (or “BK”) channel reduces EEG power in slow-wave sleep by slowing neuronal repolarization. Strikingly, this reduction completely abolishes transcriptomic changes between sleep and wake. Thus, our data establish an unexpected connection between transcription and EEG power controlled by specific potassium channels. We postulate that additive dynamic roles of individual potassium channels could integrate different influences upon sleep and wake within single neurons.

Abstract

Primary electroencephalographic (EEG) features of sleep arise in part from thalamocortical neural assemblies, and cortical potassium channels have long been thought to play a critical role. We have exploited the regionally dynamic nature of sleep EEG to develop a novel screening strategy and used it to conduct an adeno-associated virus (AAV)-mediated RNAi screen for cellular roles of 31 different voltage-gated potassium channels in modulating cortical EEG features across the circadian sleep-wake cycle. Surprisingly, a majority of channels modified only electroencephalographic frequency bands characteristic of sleep, sometimes diurnally or even in specific vigilance states. Confirming our screen for one channel, we show that depletion of the KCa1.1 (or “BK”) channel reduces EEG power in slow-wave sleep by slowing neuronal repolarization. Strikingly, this reduction completely abolishes transcriptomic changes between sleep and wake. Thus, our data establish an unexpected connection between transcription and EEG power controlled by specific potassium channels. We postulate that additive dynamic roles of individual potassium channels could integrate different influences upon sleep and wake within single neurons.

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Children's Hospital Zurich > Medical Clinic
04 Faculty of Medicine > Institute of Pharmacology and Toxicology
07 Faculty of Science > Institute of Pharmacology and Toxicology

04 Faculty of Medicine > Psychiatric University Hospital Zurich > Department of Child and Adolescent Psychiatry
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Uncontrolled Keywords:General Biochemistry, Genetics and Molecular Biology, General Agricultural and Biological Sciences
Language:English
Date:1 September 2019
Deposited On:17 Sep 2019 14:41
Last Modified:28 Jan 2020 08:25
Publisher:Cell Press (Elsevier)
ISSN:0960-9822
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.cub.2019.07.056
Official URL:https://www.sciencedirect.com/science/article/pii/S0960982219309364?via%3Dihub
PubMed ID:31474531

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