Pre-existing variability in the regulation of non-rapid eye movement sleep predicts resilience to social-defeat stress.

Preoptic area of the hypothalamus is important for the homeostatic regulation of rapid eye movement sleep.

Functional identification of GABAergic neurons in the ventral tegmental area as a important neuronal subpopulation regulating non-rapid eye movement (NREM) sleep in mice.

Multiple non-redundant features of non-rapid eye movement sleep are altered in schizophrenia and largely independent of waking electrophysiological abnormalities, supporting the promise of neuropsychiatric disease biomarkers based on a precise dissection of the sleep.

Non-oscillatory brain activity can be used to monitor arousal levels during both NREM and REM sleep as well as under general anesthesia with propofol.

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.

Cholinergic system play an important role in waking-to-sleep cycles and in sleep stabilization.

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.

Local cortical sleep features arise subcortically due to heterogeneous burst discharge in neurons of a sleep rhythm pacemaker previously thought to act uniformly.

A provoked awakening protocol during sleep reveals that selective bilateral hippocampal damage in humans is associated with reduced frequency, quality, and content of dreaming.