The study was inspired when researchers discovered that cells in the pons – an area of the brain suspected to have control of REM – actually came from the rhombic lip – a faraway area of the brain – during primary embryonic development. This prompted the researchers to assume that if they could tag rhombic lip cells, they could follow their movement to the pons and potentially artificially reboot them in the sleep phase.
The researchers employed a method known as DREADD (Designer Receptors Exclusively Activated by Designer Drugs). Using mice with expressed DREADD receptors in the rhombic lip that expressed Atoh1 in the developmental stage, researchers bound a drug to cells in the pons to monitor activity during sleep. The results showed that activated Atoh1 cells that are excited could suppress REM sleep, which could lead to complications associated with the increase of non-rapid eye movement sleep (NREM) – a much lighter phase of sleep.
Once the cells were identified, the researchers investigated the role of REM sleep on physiology. They recorded brain activity in mice during NREM sleep and shortened or elongated REM sleep. They found that slow waves, which commonly occur in NREM, became either smaller or larger. This revealed that NREM works under the control of REM sleep.
Further research by the authors will continue to use DREADD and other brain technologies to determine the evolutionary role of REM sleep in mammals in the hopes that they can unlock other mysteries.