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Sleep and wake states are not sufficient to drive changes in neocortical synaptic strengths.

New transgenic mice, which can be ablated both orexin neurons and MCH neurons, showed new brain state and revealed functional interaction that MCH neurons have protective role in narcolepsy symptoms.

Measures of sleep features such as spindles and slow waves differentiate between young people with 22q11.2 microdeletion syndrome and healthy controls, and may mediate the relationship between this genotype and psychiatric symptoms.

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

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.

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

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

Increasing cortical plasticity leads to better one-trial memory but more interference effects on semantic-like memory.

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.