New evidence supplied by scientists at UCLA proves how a gene outside the brain is responsible for enabling us to rebound from sleep deprivation. Although the news comes as quite surprising to many, it could eventually lead to enhanced treatments for insomnia patients without the need to use any drugs within the brain.
Scientists at UCLA discovered that by increasing master gene, Bmal1, that’s responsible for regulating sleep patterns, they were able to create mice that were, in fact, resistant to sleep deprivation. Senior author of the study, Ketema Paul, UCLA associate professor of integrative biology and physiology, said, “When we first saw the importance of the muscle, we were surprised. At first, we didn’t believe it, so we repeated the experiment several times. We finally realized this is not a mistake; this is real.”
It’s the first time ever that researchers have been able to prove a connection between the biological clock in muscles and the brain, and is an exciting discovery for those have trouble sleeping. Extended episodes of sleep deprivation can increase the risk for a number of illnesses including diabetes, stroke, and heart disease. So, by having a resistance to sleep loss, you may reduce the risk of contracting these ailments. The research demonstrated an impaired ability to rebound from sleep deprivation when Bmal1 was turned off through the mice’s brain and body. When the gene was restored in the skeletal muscle the mice’s ability to rebound from sleep deficit was reactivated, but when restored in the brain, it didn’t.
The research demonstrated an impaired ability to rebound from sleep deprivation when Bmal1 was turned off through the mice’s brain and body. When the gene was restored in the skeletal muscle the mice’s ability to rebound from sleep deficit was reactivated, but when restored in the brain, it didn’t.
The study suggests that skeletal muscle does, in fact, communicate directly with the brain. During one part of the study, researchers kept the mice awake for nearly 24 hours consecutively. They discovered that during this time those mice with elevated levels of Bmal1 were much less sleepy than those without the additional genes. No negative consequences could be found by increasing the Bmal1 in the muscle and is a shame we are only now revealing its true potential. Paul suggests that one reason for this may have been because we’ve always been looking to the brain for answers. He is hoping that one day in the future scientists can create a pill that raises the level of Bmal1 in the muscle. But for now, Paul is going to be taking a much deeper look into how the skeletal muscle manages to communicate with the brain.
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