Protein phosphorylation levels in the brain may drive the desire for sleep, a study published online in Nature this week suggests. The research sheds light on the molecular basis of sleep need and highlights potential molecular targets for sleep-related therapeutics.
In mammals, the sleep-wake cycle is driven by a homeostatic mechanism that balances sleep-need with sleep-taken. Qinghua Liu and colleagues studied brain protein phosphorylation levels in sleep-deprived and Sleepy mutant mouse models and found that overall phosphorylation levels were linked with sleep need. Sleep lowered phosphorylation levels, whereas prolonged wakefulness caused hyper-phosphorylation and high sleep need.
The authors identified 80 mostly synaptic proteins whose phosphorylation state changed according to sleep need. This is intriguing because synaptic plasticity has also been implicated in sleep. According to the synaptic homeostasis hypothesis, sleep gives synapses a chance to recover from their daily activity and so maintain homeostasis. Phosphorylation of synaptic proteins may therefore have a central role in maintaining both synaptic and sleep-wake homeostasis.
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