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A computational model of the thalamocortical network explains sleep stages by the coordinated variations in the level of neuromodulators and predicts differences of sleep pattern in human, cat and mouse recordings.

Different methods for inducing sleep in Drosophila flies may be promoting distinct sleep stages with different functions when brain activity and gene expression are compared.

The two most commonly used chemogenetic actuators, clozapine-N-oxide and compound 21, similarly modulate sleep in wild-type laboratory mice indicating that even designer drugs which do not convert to clozapine can elicit behavioural effects and require adequate controls.

Sub-second pontine waves functionally interact with hippocampal population activity in a state-dependent manner across sleep states, while brainstem ensemble dynamics exhibit slow, long-lasting state-predictive activity.

Whole-night fMRI-based sleep classification uncovers distinct substates within N2 and REM sleep stages, along with a transition structure between them.

Neuropathic pain preserves mouse sleep in architecture and characteristic spectral bands but perturbs arousability in ways reminiscent of insomnia disorders, in which hyperarousal and hyperalertness to environmental stimuli are prevalent.

Rostral and central striatum controls slow-wave sleep during active phase in mice.

Neurocognitive processing during sleep selectively biases subjective preferences in simple economic choices when the sleeper is stimulated by covert, reward-associated cues.

A cortical model inspired by cognitive theories and deep learning demonstrates how the combination of wakefulness, non-rapid eye movement (NREM), and REM dreams leads to the emergence of robust and semantically organized neuronal representations in higher cortical areas.

Sleep spindles, distinctive brain activity patterns occurring in non-REM sleep, modify cross-area connectivity in the motor network relevant for behavioral flexibility, impacting subsequent behavior.