Shank3, a high confidence autism gene candidate, may be a key component of the mechanisms underlying sleep problems in autism.

Cortical astrocytes play key roles in NREM sleep by regulating sleep depth and duration through separate GPCR pathways, and differentially control neuronal slow-wave activity in local and remote cortical circuits.

Irregular sleep-wake patterns are associated with higher mortality risk, including mortality due to cancer and cardiovascular disease.

Spatiotemporal manipulations of insomniac reveal that this gene regulates the birth and development of sleep-regulatory neurons, enabling their proper function in adulthood.

The transcription factor, MEF2C, mediates a change in approximately one half of the expressed frontal cortical transcriptome controlling cellular metabolism and synaptic strength in response to acute loss of sleep.

Odor cues in sleep evoke content-specific signatures of neural reactivation in visual and prefrontal brain areas that predict subsequent memory performance in the wake state.

Sleep-encoded vocabulary influences awake decision-making 36 hr later, particularly when targeting the vocabulary to slow-wave troughs, which suggests that unconscious episodic memory formation during deep sleep is possible.

The sleep–wake state sequence explains almost all of the variance in brain temperature in the mouse, and its detailed dynamics can be accurately predicted only using sleep–wake information.

Sound cues that were associated with memories during wake elicit memory reactivations when replayed to human participants during rapid eye movement sleep, those memory reactivations are identifiable by machine learning models that directly relate electroencephalography patterns of wake and sleep.

Controlling for the effects of mechanical stimulation during sleep deprivation reveals substantial multi-cycle sleep rebound in Drosophila and reveals serotonin as a potential sleep substance in the fly brain.