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According to the American Sleep Association, so many adults have sleep disorder, sleep loss compromises thinking and decision-making, which decreases work performance and productivity while increasing the risk of auto and industrial accidents. Understanding sleep regulators and effective treatments for sleeplessness.
The new research reports the first whole-brain, quantitative study of a fundamental molecular process called phosphorylation in the context of sleep need. It features a clever comparison of two different groups of tired mice: sleep-deprived normal mice and Sleepy mutant mice, a variety with a genetic mutation that confers an unusually high sleep need despite increased sleep amount.
The Sleepy mouse was identified in a collaborative study between Dr. Masashi Yanagisawa and Dr. Joseph Takahashi initiated at UT Southwestern’s Peter O’Donnell Jr. Brain Institute. Sleep need is the feeling of tiredness that builds up during waking hours, each animal exhibits a set point of total sleep time. In adult humans, that usually means about 8 out of 24 hours.
Everyone has experienced staying up too late and feeling a need to ‘make up for lost sleep. Currently, the majority of sleep medicines are mimics of GABA, an inhibitory neurotransmitter that simply shuts off the brain, and they induce nonnatural sleep with many side effects. It would be nice to understand the natural molecules better in order to design improved treatments for sleep problems.
To study the molecules involved in sleep need, researchers devised a novel strategy of comparing phosphorylation in the brains of the sleep-deprived normal mice and Sleepy mutant mice. Phosphorylation is a reversible process that modifies the functions of proteins by adding a phosphate group. The novel strategy comparing the two mice- one sleepy by circumstance, the other sleepy by nature-made it possible to exclude variables such as stress that could affect sleepiness.
Using immunochemical assays and mass spectrometry, the researchers identified 80 proteins that were hyperphosphorylated in the brains of sleep-deprived and Sleepy mice, meaning that the proteins accumulated more phosphate groups the longer the mice stayed awake. They named these proteins Sleep-Need-Index-Phosphoproteins (SNIPPs). They found that the phosphorylation of SNIPPs increased with sleep need and dissipated, or dephosphorylated, throughout the brain during sleep.
The purpose of sleep-wake balance appears to be to maximize the duration and quality of cognitive (thinking) functions of the brain. While prolonged wakefulness leads to cognitive impairment and sleepiness, sleep refreshes the brain through multiple restorative effects and optimizes cognitive functions for the next waking period. The phosphorylation cycle of SNIPPs may be an important way for the brain to reset itself every night, restoring both synaptic and sleep-wake balance to maximize clear thinking.
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