Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Sleep deprivation is a state that arises when an organism has less sleep than is optimal, and is followed by a 'rebound' in slow-wave sleep when the opportunity arises. This can be induced experimentally or environmentally (such as shift work), but is also associated with neurological and psychiatric disorders such as dementia, in which normal sleep patterns are disrupted.
Yang et al. show that moments of failed attention we experience after sleep deprivation reflect brief ‘sleep-like’ episodes in the brain, corresponding to a brain- and body-wide event with altered brain activity, pupil size and brain fluid movement.
Sleep loss has been known to increase seizure risk since antiquity, but the underlying mechanisms remain unclear. Using fruit-fly epilepsy models, the authors show that rising “sleep drive”, not sleep duration, is what triggers seizures.
Sleep disruption is a common but poorly understood feature of neurodevelopmental disorders including autism spectrum disorder. A study by Bian et al. reveals that sleep disruption in adolescent mice leads to long-lasting changes in social novelty preferences. Importantly, these perturbations can be restored through balanced actions in midbrain dopamine systems.
Fragmented sleep interferes with a novel neuroimmune axis involving hypocretin produced in the hypothalamus, leading to increased haematopoiesis and larger atherosclerotic lesions.
A set of 80 (mostly synaptic) proteins show hyperphosphorylation in sleep-deprived mice and genetically ‘sleepy’ mice, suggesting that increased phosphorylation of such proteins may be associated with sleep need.
