Researchers reveal neural switch that turns DREAMS on and off in seconds
- Were able to activate dreams in mice using laser light
- Could help treat sleep and mood disorders
Researchers have found how to induce dreams at the flick of a switch.
The team were able to activate the newly identified neurons in a mouse brain using lasers.
Within seconds, the animal entered REM sleep in a breakthrough that could have major implication in treating sleep and mood disorders in humans.
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The dream breakthrough that could have major implication in treating sleep and mood disorders in humans.
UC Berkeley neuroscientists inserted an optogenetic switch into a group of nerve cells located in the ancient part of the brain called the medulla, allowing them to activate or inactivate the neurons with laser light.
When the neurons were activated, sleeping mice entered REM sleep within seconds.
Inactivating the neurons reduced or even eliminated a mouse's ability to enter REM sleep.
'People used to think that this region of the medulla was only involved in the paralysis of skeletal muscles during REM sleep,' said lead author Yang Dan, a UC Berkeley professor of molecular and cell biology and a Howard Hughes Medical Institute Investigator.
'What we showed is that these neurons triggered all aspects of REM sleep, including muscle paralysis and the typical cortical activation that makes the brain look more awake than in non-REM sleep.'
While other types of neurons in the brainstem and hypothalamus have been shown to influence REM sleep, Dan said, 'Because of the strong induction of REM sleep – in 94 percent of the recorded trials our mice entered REM sleep within seconds of activating the neurons – we think this might be a critical node of a relatively small network that makes the decision whether you go into dream sleep or not.'
The team reported their results in Nature, and say it will not only help researchers better understand the complex control of sleep and dreaming in the brain, but will allow scientists to stop and start dreaming at will in mice to learn why we dream.
The team were able to activate the neurons in a mouse brain using lasers, sending the animal into REM sleep within seconds.
'Many psychiatric disorders, especially mood disorders, are correlated with changes in REM sleep, and some widely used drugs affect REM sleep, so it seems to be a sensitive indicator of mental and emotional health,' said first author Franz Weber, a UC Berkeley postdoctoral fellow.
'We are hoping that studying the sleep circuit might lead us to new insights into these disorders as well as neurological diseases that affect sleep, like Parkinson's and Alzheimer's diseases.'
The researchers also found that activating these brain cells while the mice were awake had no effect on wakefulness, but did make them eat more.
In normal mice, these neurons – a subset of nerve cells that release the neurotransmitter gamma-amino butyric acid (GABA), and so are called GABAergic neurons – are most active during waking periods when the mice are eating or grooming, two highly pleasurable activities.
It is believed the GABAergic neurons in the medulla have the opposite effect of stress neurons, such as the noradrenergic neurons in the pons, another ancient part of the brain.
Noradrenergic neurons release the transmitter noradrenalin, a cousin of adrenalin.
'Other people have found that noradrenergic neurons, which are active when you are running, shut down when eating or grooming.
'So it seems like when you are relaxed and enjoying yourself, the noradrenergic neurons switch off and these GABAergic neurons in the medulla turn on,' she said.
The GABAergic neurons project from the ventral part of the medulla, which sits at the top of the spinal cord, into many regions of the brainstem and hypothalamus, and thus are able to affect many bodily functions.
These regions – more primitive than the brain's cortex, the center of thinking and reasoning – are the seat of emotions and many innate behaviors as well as the control centers for muscles and automatic functions such as breathing.
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