Promoting sleep — brain, muscle or both?
Thursday, October 05, 2017
According to the Centers for Disease Control and Prevention (CDC), insufficient sleep is a public health problem, often leading to traffic accidents and occupational errors. In a 2009 survey of 74,571 adult respondents in 12 states:
- 35.3 percent reported less than seven hours of sleep during a typical 24-hour period
- 48 percent reported snoring
- 37.9 percent reported unintentionally falling asleep during the day at least once in the preceding month
- 4.7 percent reported nodding off or falling asleep while driving at least once in the preceding month
A plethora of information exists about sleep disorders, sleep deprivation and what we can do to improve our sleeping habits, such as going to bed at the same time each night and rising at the same time each morning as well as avoiding large meals, caffeine and nicotine close to bedtime.
However, understanding sleep is somewhat complex. Although we spend nearly one-third of our time sleeping (or trying to), its biological purpose remains a mystery.
One recent study that searched for answers to certain sleep disorders suggests that muscle — not brain — tissue may provide answers. Surprisingly, this finding, which was a collaboration between UT Southwestern's Peter O'Donnell Jr. Brain Institute and two other medical centers shows that a protein in the muscle can lessen the effects of sleep loss in mice.
The research demonstrates how a circadian clock protein in the muscle — BMAL1 — regulates the length and manner of sleep. While the protein's presence or absence in the brain had little effect on sleep recovery, mice with higher levels of BMAL1 in their muscles recovered from sleep deprivation more quickly. In addition, removing BMAL1 from the muscle severely disrupted normal sleep, leading to an increased need for sleep, deeper sleep and a reduced ability to recover.
Another recent study showed the unexpected presence of a type of neuron in the brains of mice that may play a central role in promoting sleep by turning off wake-promoting neurons in newly identified brain cells located in the zona incerta of the hypothalamus.
According to Seth Blackshaw, Ph.D., professor of neuroscience at the Johns Hopkins University School of Medicine, the study's lead author, understanding the brain's genetics and chemistry in mice should advance knowledge of what happens in people's brains, because the hypothalamus is an ancient system that was relatively well-conserved in evolution from fish to humans.
Wake-promoting cell types include hypocretin and GABA (γ-aminobutyric-acid)-releasing neurons of the lateral hypothalamus, which promote the transition to wakefulness from nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. This study shows that a subset of GABAergic neurons in the mouse ventral zona incerta, which express the LIM homeodomain factor Lhx6 and are activated by sleep pressure, both directly inhibit wake-active hypocretin and GABAergic cells in the lateral hypothalamus and receive inputs from multiple sleep–wake-regulating neurons.
Conditional deletion of Lhx6 from the developing diencephalon leads to decreases in both NREM and REM sleep. Furthermore, selective activation and inhibition of Lhx6-positive neurons in the ventral zona incerta regulate sleep time in adult mice, in part through hypocretin-dependent mechanisms.
Blackshaw and colleagues note that it would be interesting to discover if these cells have functions in addition to sleep regulation. The fact that neurons that express Lhx6 promote both non-REM and REM sleep distinguishes them from other sleep-regulating cells, suggesting the possibility of developing novel drug targets to treat sleep disorders, such as insomnia and narcolepsy.
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