Sleep is fundamental for complex life and under strong homeostatic pressure. It is characteristically influenced by a range of inputs or behaviours that positively (Satiety, Warmth) or negatively (Hunger, Stress, Cold) affect its expression. These behaviours are intrinsic to sleep and encoded by distinct neuronal circuitry. Understanding these interactions is at the heart of understanding sleep.
Our behavioural drive to satisfy sleep-permissive conditions appears to be hardwired, the result of intense evolutionary pressure. These conditions may also not have equal importance. On one hand, we readily form warm microclimates, using bedding or nesting material, and strongly avoid trying to sleep cold and exposed (not to be confused with just opening a window). On the other, we have little aversion to visual stimuli after sunset, such as artificial lighting and smartphone screens, to delay our sleep and disturb the circadian pacemaker.
Some mammals and birds can enter states of hibernation or daily torpor. This seems to prioritise energy conservation over sleeping and contradict the notion that sleep is a necessary component of life. However, on closer inspection, hibernators in colder climates periodically warm up to euthermia and then appear to sleep. In addition, the fat-tailed lemur, when choosing to hibernate in warmer burrows, can maintain continuous sleep without the need for rewarming. Whether sleep is present and undetectable or inhibited in these hypothermic states, is still unclear. Perhaps the restorative effects of sleep are lost at lower temperatures?
In the wild, pectoral sandpipers prioritise mating over sleeping, in an intense three-week period. Similarly, migratory warblers adjust sleep postures to balance energy saving against predation risk. In the laboratory setting, mice have been shown to prioritise food seeking over sleeping. This behavior is apparently encoded by the energy balance neurons of the arcuate nucleus. Mice also optimise their sleep location towards warmer climates resulting in greater total sleep, in part as a result of preoptic circuitry. Lastly, some pre-sleep behaviours including “nest building” are controlled by the ventral tegmental area. These behaviours do not occur in isolation and must be integrated, but the circuitry is widely distributed across the brain. Does this allow the integration of sleep circuits with sensory inputs and motor outputs?
As sleep is linked to a colder body and brain, sedative and anaesthetic drugs are linked to hypothermia in both mice and humans. Sedatives, general anaesthetics and torpor-inducing drugs seem to mimic sleep features, reconstituting behavioural, EEG and core temperature features associated with sleep. To what extent these drugs induce sleep-states functionally equivalent to natural sleep is still an unresolved question, as is the mechanism by which they act on the neuronal circuitry of sleep control.
The goal of this Research Topic is to collect data on sleep-related behaviours and, where possible, their circuitry. We welcome Original data and Reviews from both laboratory studies and field studies, recognizing the value of comparative biology. Ultimately, we are interested in how these behaviours and associated circuitry can help us to understand the functions of sleep. Suggested topics can include, but are not limited to:
1. Neuronal basis for sleep-related behaviours or sleep-state transitions
2. Characterisations of sleep-related behaviours
3. The mechanisms of sedative drugs
4. The relationship between sleep and daily torpor or hibernation
5. How neuronal circuitry can help us understand the functions of sleep
Sleep is fundamental for complex life and under strong homeostatic pressure. It is characteristically influenced by a range of inputs or behaviours that positively (Satiety, Warmth) or negatively (Hunger, Stress, Cold) affect its expression. These behaviours are intrinsic to sleep and encoded by distinct neuronal circuitry. Understanding these interactions is at the heart of understanding sleep.
Our behavioural drive to satisfy sleep-permissive conditions appears to be hardwired, the result of intense evolutionary pressure. These conditions may also not have equal importance. On one hand, we readily form warm microclimates, using bedding or nesting material, and strongly avoid trying to sleep cold and exposed (not to be confused with just opening a window). On the other, we have little aversion to visual stimuli after sunset, such as artificial lighting and smartphone screens, to delay our sleep and disturb the circadian pacemaker.
Some mammals and birds can enter states of hibernation or daily torpor. This seems to prioritise energy conservation over sleeping and contradict the notion that sleep is a necessary component of life. However, on closer inspection, hibernators in colder climates periodically warm up to euthermia and then appear to sleep. In addition, the fat-tailed lemur, when choosing to hibernate in warmer burrows, can maintain continuous sleep without the need for rewarming. Whether sleep is present and undetectable or inhibited in these hypothermic states, is still unclear. Perhaps the restorative effects of sleep are lost at lower temperatures?
In the wild, pectoral sandpipers prioritise mating over sleeping, in an intense three-week period. Similarly, migratory warblers adjust sleep postures to balance energy saving against predation risk. In the laboratory setting, mice have been shown to prioritise food seeking over sleeping. This behavior is apparently encoded by the energy balance neurons of the arcuate nucleus. Mice also optimise their sleep location towards warmer climates resulting in greater total sleep, in part as a result of preoptic circuitry. Lastly, some pre-sleep behaviours including “nest building” are controlled by the ventral tegmental area. These behaviours do not occur in isolation and must be integrated, but the circuitry is widely distributed across the brain. Does this allow the integration of sleep circuits with sensory inputs and motor outputs?
As sleep is linked to a colder body and brain, sedative and anaesthetic drugs are linked to hypothermia in both mice and humans. Sedatives, general anaesthetics and torpor-inducing drugs seem to mimic sleep features, reconstituting behavioural, EEG and core temperature features associated with sleep. To what extent these drugs induce sleep-states functionally equivalent to natural sleep is still an unresolved question, as is the mechanism by which they act on the neuronal circuitry of sleep control.
The goal of this Research Topic is to collect data on sleep-related behaviours and, where possible, their circuitry. We welcome Original data and Reviews from both laboratory studies and field studies, recognizing the value of comparative biology. Ultimately, we are interested in how these behaviours and associated circuitry can help us to understand the functions of sleep. Suggested topics can include, but are not limited to:
1. Neuronal basis for sleep-related behaviours or sleep-state transitions
2. Characterisations of sleep-related behaviours
3. The mechanisms of sedative drugs
4. The relationship between sleep and daily torpor or hibernation
5. How neuronal circuitry can help us understand the functions of sleep
