A new study, published in the July 18 edition of The Journal of Neuroscience, has discovered a way to help researchers gain a better understanding and to offer better treatment for sleep disorders, such as REM sleep behavior disorder, narcolepsy and tooth grinding. The study discovered that two powerful brain chemical systems work jointly to paralyze skeletal muscles during rapid eye movement (REM) sleep.

During REM sleep, i.e. the sleeping phase in which most dreams we recall occur, muscles that allow eye movement and breathing continue to move, whilst the majority of other muscles are prevented from moving, which may be due to prevent injury.

Toronto University’s neuroscientists Patricia L. Brooks and John H. Peever, PhD, discovered in various rat experiments that the neurotransmitters gamma-aminobutyric acid (GABA) and glycine caused REM sleep paralysis by “switching off” special brain cells that control muscle activity. The discovery revokes previous beliefs of glycine being the sole inhibitor of these motor neurons.

Dennis J. McGinty, PhD, a behavioral neuroscientist and sleep researcher from the University of California in L.A. commented:

“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. 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.” McGinty was not involved in the study.

The researchers measured electrical activity in the facial muscles that are responsible for chewing of sleeping rats, which are controlled by trigeminal motor neurons (a type of brain cell) that transmits the brain’s message to activate movement in these muscles. Earlier studies indicated that REM sleep paralysis is caused by ionotropic GABAA/glycine receptors, i.e. neurotransmitter receptors in the motor neurons, yet when the team inhibited these receptors, they discovered that REM sleep paralysis still occurred.

To prevent REM sleep paralysis, the team had to inhibit both the GABAA/glycine ionotropic receptors and a different receptor system, called metabotropic GABAB receptors. This means by cutting off the motor cells from all sources of GABA and glycine no paralysis occured, which enabled high levels of muscle activity in the animals when their muscles should have been inactive, which indicates that instead of working separately, the two neurotransmitters must both be present together to maintain motor control during sleep.

The discovery could be particularly beneficial for people suffering from REM sleep disorder, a condition, which causes people to act out their dreams and which can lead to serious injuries to the patients themselves as well as to others. REM sleep disorder is also frequently an early indicator of neurodegenerative diseases like Parkinson’s disease.

Peever concluded:

“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. REM sleep behavior disorder could be an early marker of these diseases, and curing it may help prevent or even stop their development.”

Written by Grace Rattue