Duncan NRI Faculty and Staff Publications

Language

English

Publication Date

7-29-2025

Journal

Nature Communications

DOI

10.1038/s41467-025-62311-x

PMID

40730814

PMCID

PMC12307685

PubMedCentral® Posted Date

7-29-2025

PubMedCentral® Full Text Version

Post-print

Abstract

Sleep loss has been associated with increased seizure risk since antiquity. Using automated video detection of spontaneous seizures in Drosophila epilepsy models, we show that seizures worsen only when sleep restriction raises homeostatic "sleep drive," not simply when total sleep amount falls. This is supported by the paradoxical finding that acute activation of sleep-promoting circuits worsens seizures, because it increases sleep drive without changing sleep amount. Sleep-promoting circuits become hyperactive after sleep loss and are associated with increased whole-brain activity. During sleep restriction, optogenetic inhibition of sleep-promoting circuits to reduce sleep drive protects against seizures. Downregulation of the 5HT1A serotonin receptor in sleep-promoting cells mediates the effect of sleep drive on seizures, and we identify an FDA-approved 5HT1A agonist to mitigate seizures. Our findings demonstrate that while homeostatic sleep is needed to recoup lost sleep, sleep drive comes at the cost of increasing seizure susceptibility.

Keywords

Animals, Seizures, Sleep, Sleep Deprivation, Disease Models, Animal, Brain, Drosophila melanogaster, Receptor, Serotonin, 5-HT1A, Optogenetics, Homeostasis, Male, Drosophila Proteins, leep deprivation, Epilepsy

Published Open-Access

yes

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