Sleeping is often considered one of the most primitive and mundane aspects of biological existence. Some scientists claim that it is a survival instinct that has evolved for millions of years. However, despite its ancestral roots, sleep is not very well understood. In fact, countless mysteries take place when we sleep: How does the mind create dreams? Do dreams come in colors or black-and-white? Most importantly, how does the brain sustain and maintain high levels of activity during certain periods of the sleep cycle?
Each of these underlying processes is governed by a variety of complex physiological mechanisms. In particular, the stage of sleep in higher vertebrates referred to as the rapid eye movement (REM) cycle is directly correlated to dream-making. The REM cycle is unique in that it puts the brain in a state of active alertness that almost mimics wakefulness.
Recently, a group of international researchers at the RIKEN Center for Biosystems Dynamics Research (BDR) in Japan have identified two genes that appear to be key regulators of REM sleep.
The research team, led by University of Tokyo Professor Hiroki Ueda, was aware from previous studies that acetylcholine and its receptors might play a role in inducing REM sleep. The brain often releases surges of acetylcholine during REM, but scientists could not pinpoint which genes were at the receiving end of this neural network.
Equipped with the knowledge of acetylcholine and its potential receptors, the researchers turned to large-scale genetic screening in mice in search of the specific acetylcholine receptors.
They knocked out different genes encoding a variety of acetylcholine receptors and as a result, found that the absence of two acetylcholine receptors, Chrm1 and Chrm3, cause the elimination of REM sleep in mouse models. In other words, Chrm1 and Chrm3 are indispensable in bringing about the onset of the REM cycle.
Chrm1 and Chrm3 had never been extensively studied prior to this discovery, but researchers are currently aware that they are distributed over a wide range of distinct regions in the brain. More specifically, Chrm1 is somehow responsible for coordinating smooth and unfragmented REM sleep while Chrm3 is responsible for maintaining the length of REM sleep.
To the researchers’ further surprise, when Chrm1 and Chrm3 were knocked out concurrently in mice, the mice were able to survive despite the lack of REM sleep.
Yasutaka Niwa, the co-first author of the article, expressed his excitement for the new discovery in a press release.
“The surprising finding that mice are viable despite the almost complete loss of REM sleep will allow us to rigorously verify whether REM sleep plays a crucial role in fundamental biological functions such as learning and memory,” Niwa said.
Shakira King, a junior at Hopkins majoring in Neuroscience, also expressed her surprise during an interview with The News-Letter.
“I remember learning about acetylcholine and sleep as two completely separate topics in the Neuroscience course here at Hopkins. I would have never thought that acetylcholine also plays a critical role in REM sleep, but this research goes to show that neurotransmitters may actually be much more versatile than we currently think,” King said. “It’s also a testament to the fact that our understanding of the nervous system is constantly evolving and there’s so much more for us to discover about the hidden complexities of this body system.”
The researchers recently published the results of their study in Cell Reports on August 28. The implications of this study are particularly exciting for the realms of neuroscience and sleep psychology, as scientists can now move on to study the cellular mechanisms of REM and unfold questions in the field that have long remained unanswered.
