The Happy Hormone Dopamine May Guide the Brain’s Entry Into Dreams (2024)

Thank you. Listen to this article using the player above. ✖

Technology Networks Ltd. needs the contact information you provide to us to contact you about our products and services. You may unsubscribe from these communications at any time. For information on how to unsubscribe, as well as our privacy practices and commitment to protecting your privacy, check out our Privacy Policy

A surprising set of findings has implicated the “happy hormone” dopamine as having a central role in our brains’ switch into rapid-eye-movement (REM) sleep, the part of our sleep cycle during which we dream.

The mystery of why we sleep

We all spend a large chunk of our lives sleeping and dreaming. Science still hasn’t really produced a full answer as to why our brains require a period of unresponsive lying down every day and why our brains show us vivid visions of unreality for a portion of that time, but researchers have gone some ways towards working out the how of sleep. Previous studies have tracked the ebb and flow of neurotransmitter tides through specific brain areas. Many of these tides follow a similar pattern: a neuron-soaking flood during wakefulness, followed by a molecular trickle during non-REM sleep and a drought during REM sleep.

But a 2016 study highlighted that a group of neurons in a region of our brainstem called the ventral tegmental area (VTA) weren’t following the script on sleep. These cells, which release dopamine, the so-called “happy hormone” that plays a key role in our reward and motivation systems, appeared to ramp up activity during dreaming.

These initial findings prompted new analyses, authored by Emi Hasegawa and colleagues from the University of Tsukuba, published in Science today (March 3).

Molecular tools to analyze sleep

Hasegawa and team looked at several brain regions that receive the signals produced by these out-of-rhythm cells and used a selection of molecular tools to examine how they functioned during sleep.

They identified in mice that neurons in the basolateral amygdala (BLA), a center of emotion processing in the brain, fired themselves up just before the brain transitioned to REM sleep.

By using a technique called optogenetics, the group were able to activate these cells while the mice were in non-REM sleep. This activation sent the mice into dreams after just a couple of minutes, while control mice took nearly 10 minutes to enter REM sleep. The researchers were able to trace a molecular path through this, showing that when cells in the VTA fire onto the BLA, cells expressing the dopamine receptor D2 (DRD2) are inhibited. This in turn unshackles pathways that flow out from the BLA, which stimulate the transition to REM sleep.

What Is Optogenetics?

Optogenetics is a technique, primarily used in neuromodulation, that gives researchers control over the activity of neurons or other cells or groups of cells. Animals are genetically modified so that some of their neurons express light-sensitive ion channels, allowing cell function to be turned on or off in response to light exposure.

When the sleep cycle loses its rhythm

While we all require sleep, for some people, its intrusion into waking life can cause significant problems. Narcolepsy is a chronic condition where people lose regulation over their sleep–wake cycles, sending them into REM sleep without warning. One feature of narcolepsy is cataplexy, where the switch to REM sleep causes patients to lose motor control. The team decided to examine how their putative REM-inducing neurons functioned in mice which had been genetically manipulated to induce narcolepsy. They showed that prior to cataplectic attacks, the mice’s brains flooded dopamine into the BLA. Their brains also produced a higher volume of dopamine than those of their non-narcoleptic litter-mates.

The team were even able to induce cataplexic events in mice without narcolepsy simply by inhibiting the BLA neurons using the optogenetic stimulation they had trialed earlier in the study. In a Perspectives piece released in the same issue of Science, Professors Elda Arrigoni and Patrick Fuller, from Harvard Medical School and the University of California, Davis School of Medicine respectively, commented on this finding. “This is a striking finding and one that may require a reconsideration of the prevailing neurobiological models of cataplexy in the context of narcolepsy,” they wrote.

Arrigoni and Fuller also highlighted that the story of sleep in the brain remains incomplete. Previous studies have identified that activity in other regions of the brainstem, such as the pons and medulla, are essential for REM sleep, but there appear to be no obvious connections between the BLA neurons identified by Hasegawa and team and these other regions.

Dopamine is a hugely important neurotransmitter that can be modified using commercially available compounds like modafinil, which is already available as a medication for sleep disorders. Arrigoni and Fuller point out that drugs like modafinil, while boosting wakefulness, appear to have no effects on REM sleep. The new research from Hasegawa and colleagues, however, suggests that new drugs targeting the BLA could provide relief for sleep disorder patients, even if the findings only add to the mystery of why we dream.

Reference:

Hasegawa, E, Miyasaka, A, Sakurai, K, Cherasse, Y, Li, Y and Sakurai, T. Rapid eye movement sleep is initiated by basolateral amygdala dopamine signaling in mice. Science. 2022;375(6584):994-1000. doi: 10.1126/science.abl6618