Parkinson’s disease is a neurodegenerative disorder that affects Dopaminergic neurons, which are nerve cells in the brain responsible for producing dopamine. Dopamine functions as a neurotransmitter...
According to Stephanie Pappas, Live Science contributor, our dreams may come from two genes. A new study in mice found that these dream genes are essential for our phase of slumber that brings people some bizarro-world visions of taking high school math tests naked, losing teeth and soaring through the air.
Without the genes that are called Chrm 1 and Chrm 3, mammals wouldn’t experience their rapid eye movement (or REM sleep) when the brain is as active as it is during our wakefulness but the body is paralyzed. Researchers believe the discovery is important as poor sleep and psychiatric disorders are linked. Understanding the control of sleep in the brain might be able to refine pharmaceutical treatments for sleep and psychiatric problems, according to study leader Hiroki Ueda of Riken, a Japanese research institute.
It is absolutely essential having sound sleep for our quality of human life. Some impairment in sleep may lead to various unexpected consequences. The molecular machinery can hinder the development of treatments for sleep-related diseases.
In any night, humans cycle through non-rem and rem sleep, which are different patterns of brain activity. The reason for these different sleep phases are unknown, but REM sleep has been linked to dementia, Parkinson’s disease and other neurological disorders. An increased risk of suicide is linked to problems with REM sleep.
This is the main reason why Ueda and colleagues are interested in understanding the basics of how our sleep works. Transition from non-REM to REM sleep involves a neurotransmitter called acetylcholine. Researchers used CRISPR technology to work out the genes for these acetylcholine receptors in mice. It uses a genetic sequence to guide an enzyme to the specific sections of DNA and the enzyme snips the sequence, preventing that gene from being expressed.
The receptors Chrm 1 and Chrm 3 shortened sleep by close to 3 hours a day. Losing one or the two receptors reduced and fragmented REM sleep specifically. It also reduced non-REM sleep. REM-free mice survived without the dreamy sleep state, even though the hypotheses is that sleep is necessary for survival. Mutant mice can survive in a lab condition with a lot of food and without any enemies.
If we can understand the specific receptors controlling our sleep, we can inform new treatment for psychiatric disorders like depression and PTSD, which is often full of vivid nightmares. They did find subtle differences the way Chrm 1 and Chrm 3 work, so they are interested in taking a closer look at what happens when these two receptors are triggered. This may help molecularly defined REM sleep and might reveal the physiological roles of REM sleep in related higher cognitive functions, such as learning and memory, according to Ueda.
Dr Fredda Branyon