When you think of dopamine, pleasure and addiction are usually the first two reactions. But think again. Well, dream again: The neurotransmitter plays a role in activating sleepy dreams.
Researchers found that increased levels of dopamine in an important part of the brain helped mice make the transition from non-rapid eye movement, or NREM, to REM sleep, the portion of the night where your dreams typically happen. A team led by the University of Tsukuba published its findings this month in the journal Science.
The findings could point to a new drug target for REM sleep disorders and potentially Parkinson's disease, because dopamine signaling is disrupted in that neurodegenerative condition, neurology professors from Harvard and the University of California wrote in a related perspective piece.
Dopamine was increasingly activated in the basolateral amygdala region of the mice's brain in the build up to REM sleep but not before NREM transitioned back to a waking state, according to the researchers at the University of Tsukuba.
The researchers wanted to know whether dopamine also played a role in triggering cataplexy. The sudden loss of muscle control is a sign of the sleeping disorder narcolepsy, which disrupts REM sleep and causes drowsiness throughout the day.
In mice with the sleeping disorder, researchers at the Japanese university found dopamine levels in the basolateral amygdala increased before the muscle weakness attacks.
The researchers used optogenetic manipulation, in which they help excite light-sensitive ion channels to manipulate neurons to excite the dopamine fibers in the basolateral amygdala when the mice were in NREM sleep. That caused the animals to switch to REM sleep, they found. The brain region communicates with other parts of the brain that impact cognition, motivation and stress responses.
One commonly used treatment to help relieve sleeping disorders is melatonin, which works by regulating the biological clock. The neurohormone interacts with cellular receptors to ease the sleep-wake cycle.
Researchers at the University of Southern California mapped the structures behind the two key melatonin receptors, MT1 and MT2. The findings led to a better understanding of how to design druglike molecules that would bind to one receptor rather than both so it minimizes unwanted side effects.