Two genes are able to control how much we dream, new research has shown.
The findings, published in the journal Cell Reports, provide insight into the molecular mechanisms of REM sleep.
Humans and other animals cycle through two major stages of sleep: Rapid Eye Movement (REM) sleep, which is when dreaming occurs, and non-REM sleep.
During REM sleep, neural activity more closely resembles that of a fully awake brain. Moreover, a number of studies suggest that the REM stage may contribute to our ability to consolidate memories as we sleep. Nevertheless, the relationship between dreaming and our cognitive function remains unclear and, to date, it is still not known exactly why we dream, or how.
Increasing evidence suggests that the neurotransmitter acetylcholine may play a crucial role in REM sleep. Specifically, it has been shown that high levels of it are released in some regions of the mammalian brain both during REM sleep and wakefulness, but it’s not known what regulates this.{%recommended 5992%}
Now, an international team of researchers led by Hiroki Ueda at the RIKEN Centre for Biosystems Dynamics Research (BDR) and the University of Tokyo, both in Japan, have identified two genes that play a critical role in this process.
The researchers were able to systematically switch off expression of a variety of genes for acetylcholine receptors in mice. In so doing, they discovered that disabling two genes in particular, Chrm1 and Chrm3, significantly affected sleep behaviour.
Disabling Chrm1 alone caused the mice to experience reduced and fragmented REM sleep, while disabling Chrm3 alone reduced the length of non-REM sleep. The most striking result came when both genes were knocked out at the same time: the mice almost entirely lost their capacity to experience REM sleep.
This suggests that Chrm1 and Chrm3 are necessary for regulation of REM sleep, though most likely play different roles in that process.
“The discovery that Chrm1 and Chrm3 play a key role in REM sleep opens the way to studying its underlying cellular and molecular mechanisms and will eventually allow us to define the state of REM sleep, which has been paradoxical and mysterious since its original report,” says Ueda.
Yasutaka Niwa, a first author on the study, notes that while the loss of both receptors left the mice essentially unable to dream, it did not affect their survival.
“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,” he says.
