Polysomnographical analysis in humans shows that temporal fluctuations of aperiodic neural activity reflect the cycling nature of sleep.

Sleep spindles provide a temporal framework to organize the reactivation of behaviorally relevant CA1 cells and sparsely active cells in the limbic thalamus.

Using long-term in vivo imaging with miniature two-photon microscopy, microglia surveillance is sleep state-dependent and stress-induced in freely behaving mice, regulated by the locus coeruleus-norepinephrine system and β₂-adrenergic receptors signaling.

Dynamic calcium activity in the hippocampus changes markedly across behavioral and physiological states and depends on muscarinic acetylcholine receptor activation.

Sleep-wake patterns, together with a suprachiasmatic nuclei-independent circadian factor, are necessary and sufficient to maintain high-amplitude nychthemeral rhythms in PERIOD-2.

A gene found in Drosophila, and named redeye, encodes a protein that accumulates during sleep deprivation and forms part of the homeostatic system that promotes and maintains 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.

Drosophila grooming is driven by two internal programs.

A missense mutation in the human Cryptochrome 2 (CRY2) gene leads to the condition of familial advanced sleep phase.

An internal clock based on brain levels of dopamine works with the circadian clock to maintain daily patterns of alertness and activity, and may be implicated in the altered behavioral patterns seen in schizophrenia and bipolar disorder.