How much REM and non-REM sleep we get appears to be controlled by a pair of genes.
“Dream a little gene of me,” doesn’t have quite the same lyrical beauty of the 1931 lyrics later made so famous by Mama Cass. But it’s accurate, according to new research from the RIKEN Center for Biosystems Dynamics Research in Japan. There, scientists have discovered that a pair of receptor genes regulate how much REM and non-REM sleep animals get.
To back up a minute, for higher vertebrate animals such as humans, sleep is grouped into two phases: REM, which stands for rapid eye movement, and non-REM. The current belief is that during REM, the brain is a busy desk clerk, filing and processing all the information we’ve taken in for the day. This is important for memory consolidation. During this phase, according to the American Sleep Association, our body acts as if it is paralyzed, except our eyes, which keep us from acting out our dreams. Otherwise, we might start surfing in bed to get away from the fuzzy yellow monster wearing Mrs. Maple’s glasses, which could get a little crazy at 2 a.m.
Researchers at RIKEN BDR and the University of Tokyo were working with mice and found that by modifying two acetylcholine receptors in their brains, Chrm1 and Chrm3, the mice pretty much stopped having REM sleep. However, the mice survived. (They probably looked terrible!) This genetic research led to two interesting conclusions. One, it strongly suggests that removing these two receptors, which are widely distributed in distinct regions of the brain, will reduce and fragment REM sleep greatly. But second, it also called into question the very role of REM sleep.
“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,” wrote Yasutaka Niwa, the study’s first author.
I don’t know… Mice might not need it, but I’m getting tired just thinking about losing REM sleep.