"Long before it's in the papers"
October 15, 2015

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Researchers find brain switch said to turn dreams on and off

Oct. 15, 2015
Courtesy of University of California - Berkeley
and World Science staff

Neu­ro­sci­en­tists now say they can send a sleep­ing mouse in­to dream­land at the flip of a switch.

The re­search­ers in­sert­ed a de­vice called an op­to­ge­netic switch in­to a group of neu­rons, or nerve cells, in an an­cient part of the brain called the me­dul­la. This let them ac­ti­vate or inac­ti­vate the cells with la­ser light.

When a la­ser trig­gers an op­to­ge­netic switch in cells in the me­dul­la of a sleep­ing mouse, the an­i­mal goes from non-REM sleep (NREM) in­to REM or dream sleep, ac­cord­ing to re­search­ers. Ex­ten­sions of these cells called ax­ons (green) reach in­to dis­tant parts of the prim­i­tive brain. (Cred­it: Franz We­ber/UC Berke­ley )


Up­on ac­tiv­ati­on, they said, sleep­ing mice en­tered what’s known as REM sleep—the dream­ing stage—with­in sec­onds. 

REM sleep, char­ac­ter­ized by rap­id eye move­ments, fea­tures ac­tiv­ati­on of the cor­tex, or the out­er, “think­ing” part of the brain. It al­so in­volves to­tal pa­ral­y­sis of the skele­tal mus­cles, pre­sumably so that we don’t act out our dreams.

Inac­tivating the cells, on the oth­er hand, re­duced or elim­i­nat­ed a mouse’s abil­ity to en­ter REM sleep, the sci­en­tists said.

“Peo­ple used to think that this re­gi­on of the me­dul­la was only in­volved in the pa­ral­y­sis of skele­tal mus­cles dur­ing REM sleep,” said Yang Dan of the Un­ivers­ity of Cal­i­for­nia, Berke­ley, lead au­thor of a re­port on the find­ings. 

“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 else­where in the brain 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 the Oct. 15 print is­sue of the jour­nal Na­ture, and the pa­per was posted on­line Oct. 7.

Although no one knows exactly what animals might dream about, a study published earlier this year suggested rats may dream about finding treats.

The find­ing about the “switch” will not only help re­search­ers bet­ter un­der­stand the com­plex con­trol of sleep and dream­ing in the brain, the re­search­ers said, but will al­low sci­en­tists to stop and start dream­ing at will in mice to learn why we dream.

“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 co-au­thor Franz We­ber, al­so of UC Berke­ley. “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 cells that re­lease a mes­sen­ger mol­e­cule called gamma-amino bu­tyr­ic ac­id or GABA, and so are called GABAer­gic neu­rons—are most ac­tive dur­ing wak­ing pe­ri­ods when the mice are eat­ing or groom­ing, two pleas­ur­a­ble ac­ti­vi­ties.

Dan sus­pects that these 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. Those re­lease the mess­enger molecule nor­a­dren­a­line, 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 have ex­ten­si­ons that proj­ect from the ven­tral part of the me­dul­la, which sits at the top of the spi­nal cord, in­to oth­er re­gi­ons of the brain that are more prim­i­tive than the cor­tex, the cen­ter of think­ing and rea­son­ing. They are the seat of emo­ti­ons and many in­nate be­hav­iors as well as the con­trol cen­ters for mus­cles and au­to­mat­ic func­ti­ons such as breath­ing.

To study the cells, the re­search­ers in­sert­ed a light-sen­si­tive mo­lec­u­lar struc­ture in­to them by means of a vi­rus. This mo­lec­u­lar struc­ture, called an ion chan­nel, can turn on the ac­ti­vity of neu­rons when stim­u­lat­ed by la­ser light through an op­ti­cal fi­ber in­sert­ed in the brain. Up­on ac­tiv­ati­on, the cells start fir­ing elec­tri­cal pulses called acti­on po­ten­tials at oth­er cells in their net­work.


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Neuroscientists now say they can send a sleeping mouse into dreamland at the flip of a switch. The researchers inserted a device called an optogenetic switch into a group of neurons, or nerve cells, in an ancient part of the brain called the medulla. This let them activate or inactivate the cells with laser light. Upon activation, they said, sleeping mice entered what’s known as REM sleep—the dreaming stage—within seconds. REM sleep, characterized by rapid eye movements, is accompanied by activation of the cortex, or the outer, “thinking” part of the brain. It also involves total paralysis of the skeletal muscles, presumably so that we don’t act out our dreams. Inactivating the cells, on the other hand, reduced or eliminated a mouse’s ability to enter REM sleep, the scientists said. “People used to think that this region of the medulla was only involved in the paralysis of skeletal muscles during REM sleep,” said Yang Dan of the University of California, Berkeley, lead author of a report on the findings. “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 elsewhere in the brain 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 the Oct. 15 print issue of the British journal Nature, and the paper was posted online Oct. 7. The finding will not only help researchers better understand the complex control of sleep and dreaming in the brain, the researchers said, but will allow scientists to stop and start dreaming at will in mice to learn why we dream. “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 co-author Franz Weber, also of UC Berkeley. “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 cells that release a messenger molecule called gamma-amino butyric acid or GABA, and so are called GABAergic neurons—are most active during waking periods when the mice are eating or grooming, two pleasurable activities. Dan suspects that these 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 have extensions that project from the ventral part of the medulla, which sits at the top of the spinal cord, into other regions of the brain that are more primitive than the cortex, the center of thinking and reasoning. They are the seat of emotions and many innate behaviors as well as the control centers for muscles and automatic functions such as breathing. To study the cells, the researchers inserted a light-sensitive molecular structure into them by means of a virus. This molecular structure, called an ion channel, can turn on the activity of neurons when stimulated by laser light through an optical fiber inserted in the brain. Upon activation, the cells start firing electrical pulses called action potentials at other cells in their network.