Muscles Paralyzed During Sleep
redOrbit Staff & Wire Reports – Your Universe Online
Finding may suggest new treatments for sleep disorders
Understanding sleep disorders including REM sleep behavior disorder, narcolepsy and grinding of the teeth could be linked to two strong brain chemicals and a system network that works together to stop rapid eye movement and muscle movement during sleep. New research in the July 18 issue of The Journal of Neuroscience may help scientists better understand and treat sleep disorders.
During REM sleep, the deep sleep where most recalled dreams occur, muscles that move the eyes and those involved in breathing continue to move, but the most of the body’s other muscles are stopped in order to prevent injury. In a series of experiments, University of Toronto neuroscientists Patricia L. Brooks and John H. Peever, PhD, found that the neurotransmitters gamma-aminobutyric acid (GABA) and glycine caused REM sleep paralysis in rats by “switching off” the specific cells in the brain that allow muscles to be moving. This finding reversed earlier beliefs that glycine was the only inhibitor of these motor neurons.
“The study’s findings are relevant to anyone who has ever watched a sleeping pet twitch, gotten kicked by a bed partner, or has known someone with the sleep disorder narcolepsy,” said Dennis J. McGinty, PhD, a behavioral neuroscientist and sleep researcher at the University of California, Los Angeles, who was not involved in the study. “By identifying the neurotransmitters and receptors involved in sleep-related paralysis, this study points us to possible molecular targets for developing treatments for sleep-related motor disorders, which can often be debilitating,” he said.
The researchers measured electrical activity in the facial muscles responsible for chewing in sleeping rats. Brain cells called trigeminal motor neurons communicate the brain’s message to move to these muscles. Previous research thought neurotransmitter receptors called ionotropic GABAA/glycine receptors in the motor neurons caused REM sleep paralysis. However, when the researchers blocked these receptors, REM sleep paralysis still took place.
The researchers found that to prevent REM sleep paralysis, they had to block the GABAA/glycine ionotropic receptors and metabotropic GABAB receptors, a different receptor system. In other words, when the motor cells were cut off from all sources of GABA and glycine, the paralysis did not occur, allowing the rats to exhibit high levels of muscle activity when their muscles should have been inactive. The data suggest the two neurotransmitters must both be present together to maintain motor control during sleep, rather than working separately.
The finding could be especially helpful for those with REM sleep disorder, a disease that causes people to act out their dreams. This can cause serious injuries to patients and others around them. It is also often an early indicator of neurodegenerative diseases, such as Parkinson’s.
“Understanding the precise mechanism behind these chemicals’ role in REM sleep disorder is particularly important because about 80 percent of people who have it eventually develop a neurodegenerative disease, such as Parkinson’s disease,” study author Peever added. “REM sleep behavior disorder could be an early marker of these diseases, and curing it may help prevent or even stop their development,” he said.