A number of findings has revealed that the happy hormone dopamine is putting a key role in our brains moving into rapid-eye-movement (REM) sleep, the process in which we dream.
The mystery of why we sleep
We all spend a significant portion of our lives sleeping and dreaming. Science hasnt really provided a clear answer as to why our brains require a period of unresponsive lying down every day, and why our brains show us vivid senses of unreality for a portion of that time, but scientists have gone some steps toward understanding the meaning of sleep. Many of these methods have been used in conjunction with a molecular trickle during non-REM sleep and a drought during REM sleep.
A 2016 study reveals that a group of neurons in a neural network known as the ventral tegmental area (VTA) weren''t following the instructions on sleep. These cells, which release dopamine, the so-called happy hormone, appeared to increase activity during dreaming.
New research was prompted by Emi Hasegawa and colleagues from the University of Tsukuba, authored today (March 3).
Molecular tools to analyze sleep
Hasegawa and his team explored several brain regions that receive the signals from these out-of-rhythm cells and used a variety of molecular tools to evaluate how they functioned during sleep.
neurons in the basolateral amygdala (BLA), a brain processing center, were identified just before the brain transitioned to REM sleep.
Using a technique called optogenetics, the group was able to activate these cells while the mice were in non-REM sleep. This activation sent the mice into dreams after a couple of minutes, and control mice took nearly 10 minutes to enter REM sleep. This allows the researchers to further uncover a molecular path through which shows that when cells in the VTA fire onto the BLA, cells expressing the dopamine receptor D2 (DRD2) are inhibited. This leads to the transition to
What Is Optogenetics?
Optogenetics is a technique that enables researchers to control the activity of neurons or other cells or groups of cells. Animals are genetically altered so that some of their neurons express light-sensitive ion channels, allowing cell function to be switched on or off in response to light exposure.
When the sleep cycle loses its rhythm
The racial condition where people lose control of their sleepwake cycles, which can result in severe sleep disturbance. The team decided to investigate how their putative REM-inducing neurons acted in mice that had been genetically altered to induce narcolepsy. They found that before that brains injected dopamine into the BLA, they produced a higher volume of dopamine than their non-narcoleptic litter-mates.
According to the authors, the team was even able to induce cataplexic events in mice without narcolepsy by inhibiting the BLA neurons, which they had previously used in the study. This is a striking conclusion, which may require a review of the prevailing neurobiological models of cataplexy in the context of narcolepsy.
Arrigoni and Fuller have also revealed that sleep in the brain remains incomplete. Several studies have found that activity in other regions of the brainstem, such as the pons and medulla, are essential for REM sleep, although there appears to be no connections between the BLA neurons identified by Hasegawa and the team and these other regions.
Dopamine is a hugely important neurotransmitter that can be modified with commercially available compounds like modafinil, which is already available as a medication for sleep disorders. According to Arrigoni and Fuller, medications like modafinil, although boosting wakefulness, appear to have no effects on REM sleep. Even if the findings only add to the basis of our dreams, new therapies would be beneficial.
Hasegawa, E, Miyasaka, A, Sakurai, K, Cherasse, Y, Li, Y, and Sakurai, T. Basolateral amygdala dopamine signaling in mice. Science. 2022;375(6584):994-1000. doi: 10.1126/science.abl6618