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Disrupted temperature-sleep coupling mechanism in a Dravet syndrome mouse model
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Disrupted temperature-sleep coupling mechanism in a Dravet syndrome mouse model

Saja Fadila, Georgii Krivoshein, Hala Majadly, Anat Mavashov, Shahak Ranen, Marina Brusel, Iria G Dopeso-Reyes, Bertrand Beucher, Eric J Kremer, Else A Tolner, …
Nature communications, Vol.17(1), p.3232
26/02/2026
PMID: 41748557

Résumé

Animals Body Temperature - physiology Body Temperature Regulation - physiology Disease Models, Animal Epilepsies, Myoclonic - genetics Epilepsies, Myoclonic - physiopathology Female Hypothalamus - metabolism Hypothalamus - physiopathology Male Mice Mice, Inbred C57BL Mice, Transgenic NAV1.1 Voltage-Gated Sodium Channel - genetics NAV1.1 Voltage-Gated Sodium Channel - metabolism Sleep - physiology Wakefulness - physiology
Dravet syndrome (DS) is associated with epilepsy, developmental delays, thermal dysregulation, and sleep disturbances. While seizures have been linked to hippocampal dysfunction, what drives sleep disturbances and thermal dysregulation is poorly understood. Using DS mice (Scn1a ), we identified a link between sleep and thermoregulation. We found that DS mice exhibited lower core body temperature. Next, using electrocorticography, local field potential recordings, and core temperature monitoring, we showed that DS mice exhibited a lack of core temperature change during the transition from waking to non-rapid eye movement sleep. This is in contrast to wild-type (WT) mice, in which sleep onset coincided with a temperature drop. Additionally, warmth promoted sleep in WT, but not in DS mice. Vector-mediated expression of SCN1A or chemogenetic stimulation of the anterior hypothalamus restored the warmth-induced somnogenesis in DS mice. These findings highlight a connection between sleep and thermal dysregulation in DS, implicating altered neuronal activity of the hypothalamus.

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