Sound Waves Enhance Deep Sleep and Memory

Summary: Gentle noise stimulation can enhance sleep quality and improve memory in older people, a new study reports.

Source: Northwestern University.

Pink noise synced to brain waves deepens sleep and boosts memory in older adults.

Gentle sound stimulation — such as the rush of a waterfall — synchronized to the rhythm of brain waves significantly enhanced deep sleep in older adults and improved their ability to recall words, reports a new Northwestern Medicine study.

Deep sleep is critical for memory consolidation. But beginning in middle age, deep sleep decreases substantially, which scientists believe contributes to memory loss in aging.

The sound stimulation significantly enhanced deep sleep in participants and their scores on a memory test.

“This is an innovative, simple and safe non-medication approach that may help improve brain health,” said senior author Dr. Phyllis Zee, professor of neurology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine sleep specialist. “This is a potential tool for enhancing memory in older populations and attenuating normal age-related memory decline.”

The study was published March 8 in Frontiers in Human Neuroscience.

In the study, 13 participants 60 and older received one night of acoustic stimulation and one night of sham stimulation. The sham stimulation procedure was identical to the acoustic one, but participants did not hear any noise during sleep. For both the sham and acoustic stimulation sessions, the individuals took a memory test at night and again the next morning. Recall ability after the sham stimulation generally improved on the morning test by a few percent. However, the average improvement was three times larger after pink-noise stimulation.

The older adults were recruited from the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern.

The degree of slow wave sleep enhancement was related to the degree of memory improvement, suggesting slow wave sleep remains important for memory, even in old age.

Although the Northwestern scientists have not yet studied the effect of repeated nights of stimulation, this method could be a viable intervention for longer-term use in the home, Zee said.

Previous research showed acoustic simulation played during deep sleep could improve memory consolidation in young people. But it has not been tested in older adults.

The new study targeted older individuals — who have much more to gain memory-wise from enhanced deep sleep — and used a novel sound system that increased the effectiveness of the sound stimulation in older populations.

The study used a new approach, which reads an individual’s brain waves in real time and locks in the gentle sound stimulation during a precise moment of neuron communication during deep sleep, which varies for each person.

During deep sleep, each brain wave or oscillation slows to about one per second compared to 10 oscillations per second during wakefulness.

Giovanni Santostasi, a study coauthor, developed an algorithm that delivers the sound during the rising portion of slow wave oscillations. This stimulation enhances synchronization of the neurons’ activity.

After the sound stimulation, the older participants’ slow waves increased during sleep.

Larger studies are needed to confirm the efficacy of this method and then “the idea is to be able to offer this for people to use at home,” said first author Nelly Papalambros, a Ph.D. student in neuroscience working in Zee’s lab. “We want to move this to long-term, at-home studies.”

Northwestern scientists, under the direction of Dr. Roneil Malkani, assistant professor of neurology at Feinberg and a Northwestern Medicine sleep specialist, are currently testing the acoustic stimulation in overnight sleep studies in patients with memory complaints. The goal is to determine whether acoustic stimulation can enhance memory in adults with mild cognitive impairment.

Previous studies conducted in individuals with mild cognitive impairment in collaboration with Ken Paller, professor of psychology at the Weinberg College of Arts and Sciences at Northwestern, have demonstrated a possible link between their sleep and their memory impairments.

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Other Northwestern authors on the study are Paller, Sandra Weintraub and Rosemary Braun.

Northwestern has a patent pending for the technology. Santostasi is a cofounder of DeepWave Technologies, Inc., which plans to commercialize the technology.

Source: Marla Paul – Northwestern University
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Acoustic Enhancement of Sleep Slow Oscillations and Concomitant Memory Improvement in Older Adults” by Nelly A. Papalambros, Giovanni Santostasi, Roneil G. Malkani, Rosemary Braun, Sandra Weintraub, Ken A. Paller and Phyllis C. Zee in Frontiers in Human Neuroscience. Published online March 8 2017 doi:10.3389/fnhum.2017.00109

Northwestern University “Sound Waves Enhance Deep Sleep and Memory.” NeuroscienceNews. NeuroscienceNews, 25 April 2017.
<http://neurosciencenews.com/pink-noise-sleep-memory-6508/&gt;.

Abstract

Acoustic Enhancement of Sleep Slow Oscillations and Concomitant Memory Improvement in Older Adults

Acoustic stimulation methods applied during sleep in young adults can increase slow wave activity (SWA) and improve sleep-dependent memory retention. It is unknown whether this approach enhances SWA and memory in older adults, who generally have reduced SWA compared to younger adults. Additionally, older adults are at risk for age-related cognitive impairment and therefore may benefit from non-invasive interventions. The aim of this study was to determine if acoustic stimulation can increase SWA and improve declarative memory in healthy older adults. Thirteen participants 60–84 years old completed one night of acoustic stimulation and one night of sham stimulation in random order.

During sleep, a real-time algorithm using an adaptive phase-locked loop modeled the phase of endogenous slow waves in midline frontopolar electroencephalographic recordings.

Pulses of pink noise were delivered when the upstate of the slow wave was predicted. Each interval of five pulses (“ON interval”) was followed by a pause of approximately equal length (“OFF interval”). SWA during the entire sleep period was similar between stimulation and sham conditions, whereas SWA and spindle activity were increased during ON intervals compared to matched periods during the sham night.

The increases in SWA and spindle activity were sustained across almost the entire five-pulse ON interval compared to matched sham periods. Verbal paired-associate memory was tested before and after sleep.

Overnight improvement in word recall was significantly greater with acoustic stimulation compared to sham and was correlated with changes in SWA between ON and OFF intervals.

Using the phase-locked-loop method to precisely target acoustic stimulation to the upstate of sleep slow oscillations, we were able to enhance SWA and improve sleep-dependent memory storage in older adults, which strengthens the theoretical link between sleep and age-related memory integrity.

“Acoustic Enhancement of Sleep Slow Oscillations and Concomitant Memory Improvement in Older Adults” by Nelly A. Papalambros, Giovanni Santostasi, Roneil G. Malkani, Rosemary Braun, Sandra Weintraub, Ken A. Paller and Phyllis C. Zee in Frontiers in Human Neuroscience. Published online March 8 2017 doi:10.3389/fnhum.2017.00109

Sleep on It: Researchers Find What Makes Memories Tick

Summary: Researchers report on how sleep deprivation affects the ability to form new memories.

Source: Univeristy of Michigan.

Scientists have known that a lack of sleep can interfere with the ability to learn and make memories. Now, a group of University of Michigan researchers have found how sleep deprivation affects memory-making in the brain.

Previously, researchers knew that depriving mice of sleep after the mice performed a task resulted in the mice forgetting aspects of that task. But researchers weren’t sure what function of the hippocampus—two seahorse-shaped structures located in the temporal lobe of the brain where many long-term memories are made—was kept from doing its job.

Now, U-M researchers have found that interfering with sleep-associated oscillations—or the rhythmic firing of neurons—in one subsection of the hippocampus is likely the culprit. Their results are published in Nature Communications.

To test the role of oscillations in memory formation, the researchers, led by graduate student Nicolette Ognjanovski, recorded the baseline hippocampal activity of a group of mice. They placed mice into a new environment, let them explore, gave them a mild foot shock, then put them back into their home cages to rest and sleep normally.

“If you return the mouse to that same structure a day or even a couple months later, they will have this very stereotyped fear response, which is that they freeze,” said Sara Aton, an assistant professor in the Department of Molecular, Cellular and Developmental Biology and senior author of the paper. “But if you sleep-deprive an animal for a few hours after that context-shock pairing, the mouse won’t remember it the next day.”

The researchers found that in normally sleeping mice, sleep-associated oscillations in a subsection of the hippocampus called CA1 were more robust after learning. They then took a new group of mice, recorded their baseline hippocampal activity and had them complete the same task. The researchers also gave these mice a drug to inhibit a small population of inhibitory neurons in CA1 that express parvalbumin.

The researchers didn’t change the sleep behavior of the animal—they slept normally. But turning off the activity of parvalbumin-expressing neurons disrupted the rhythmic firing of surrounding CA1 neurons while those animals were asleep. Suppressing the parvalbumin-expressing cells appeared to completely wipe out the normal learning-associated increase in oscillations in that section of the mouse’s hippocampus.

“There’s an old theorem called Hebb’s Law, which is, ‘Fire together, wire together,’” Aton said. “If you can get two neurons to fire with great regularity in close proximity to each other, it’s very likely you’re going to affect the strength of connections between them.”

When the neurons were kept from firing together regularly and rhythmically, the mice forgot there was any fearful association with their task.

“The dominant oscillatory activity, which is so critical for learning, is controlled by a very small number of the total cell population in the hippocampus,” said Ognjanovski, also a first author of the study. “This changes the narrative of what we understand about how networks work. The oscillations that parvalbumin cells control are linked to global network changes, or stability. Memories aren’t stored in single cells, but distributed through the network.”

The researchers also compared the stability of the neurons’ connections between the control group and the group whose sleep oscillations were disrupted. They found that not only were the connections stronger in the control group after their learning trial, but that those neuronal connections were also stronger. These changes were blocked when sleep-associated hippocampal oscillations were experimentally disrupted.

“It seems like this population of neurons that is generating rhythms in the brain during sleep is providing some informational content for reinforcing memories,” Aton said. “The rhythm itself seems to be the most critical part, and possibly why you need to have sleep in order to form these memories.”

Next, the researchers plan to test whether restoring hippocampal oscillations (mimicking the effects of sleep in CA1) is sufficient for promoting normal memory formation when mice are sleep-deprived.

ABOUT THIS MEMORY RESEARCH ARTICLE

Funding: The research was funded by the RIKEN Brain Science Institute, the Howard Hughes Medical Institute, and the JPB Foundation.

Source: Morgan Sherburne – Univeristy of Michigan
Image Source: NeuroscienceNews.com image is adapted from the University of Michigan news release.
Original Research: Full open access research for “Parvalbumin-expressing interneurons coordinate hippocampal network dynamics required for memory consolidation” by Nicolette Ognjanovski, Samantha Schaeffer, Jiaxing Wu, Sima Mofakham, Daniel Maruyama, Michal Zochowski & Sara J. Aton in Nature Communications. Published online April 6 2017 doi:10.1038/ncomms15039

Univeristy of Michigan “Sleep on It: Researchers Find What Makes Memories Tick.” NeuroscienceNews. NeuroscienceNews, 7 April 2017.
<http://neurosciencenews.com/sleep-memory-6361/&gt;.

Abstract

Parvalbumin-expressing interneurons coordinate hippocampal network dynamics required for memory consolidation

Activity in hippocampal area CA1 is essential for consolidating episodic memories, but it is unclear how CA1 activity patterns drive memory formation. We find that in the hours following single-trial contextual fear conditioning (CFC), fast-spiking interneurons (which typically express parvalbumin (PV)) show greater firing coherence with CA1 network oscillations. Post-CFC inhibition of PV+ interneurons blocks fear memory consolidation. This effect is associated with loss of two network changes associated with normal consolidation: (1) augmented sleep-associated delta (0.5–4 Hz), theta (4–12 Hz) and ripple (150–250 Hz) oscillations; and (2) stabilization of CA1 neurons’ functional connectivity patterns. Rhythmic activation of PV+ interneurons increases CA1 network coherence and leads to a sustained increase in the strength and stability of functional connections between neurons. Our results suggest that immediately following learning, PV+ interneurons drive CA1 oscillations and reactivation of CA1 ensembles, which directly promotes network plasticity and long-term memory formation.

“Parvalbumin-expressing interneurons coordinate hippocampal network dynamics required for memory consolidation” by Nicolette Ognjanovski, Samantha Schaeffer, Jiaxing Wu, Sima Mofakham, Daniel Maruyama, Michal Zochowski & Sara J. Aton in Nature Communications. Published online April 6 2017 doi:10.1038/ncomms15039

Prolonged Sleep May Predict Dementia Risk

Data from the Framingham Heart Study has shown that people who consistently sleep more than nine hours each night had double the risk of developing dementia in 10 years as compared to participants who slept for 9 hours or less.

https://www.bu.edu/buniverse/interface/embed/embed.html?v=28Zl090

The findings, which appear in the journal Neurology, also found those who slept longer had smaller brain volumes. It is believed that the number of Americans with Alzheimer’s disease and other dementias will grow each year as the size and proportion of the U.S. population age 65 and older continues to increase. By 2025 the number of people age 65 and older with Alzheimer’s disease is estimated to reach 7.1 million.

A large group of adults enrolled in the Framingham Heart Study (FHS), were asked to indicate how long they typically slept each night. Participants were then observed for 10 years to determine who developed dementia, including dementia due to Alzheimer’s disease. Researchers from BUSM then analyzed the sleep duration data and examined the risk of developing dementia.

COM-sleeping man

“Participants without a high school degree who sleep for more than 9 hours each night had six times the risk of developing dementia in 10 years as compared to participants who slept for less. These results suggest that being highly educated may protect against dementia in the presence of long sleep duration,” explained co-corresponding author Sudha Seshadri, MD, professor of neurology at BUSM and FHS senior investigator.

According to the researchers the results suggest that excessive sleep may be a symptom rather than a cause of the brain changes that occur with dementia. Therefore, interventions to restrict sleep duration are unlikely to reduce the risk of dementia.

“Self-reported sleep duration may be a useful clinical tool to help predict persons at risk of progressing to clinical dementia within 10 years. Persons reporting long sleep time may warrant assessment and monitoring for problems with thinking and memory,” added co-corresponding author Matthew Pase, PhD, fellow in the department of neurology at BUSM and investigator at the FHS.

The researchers believe screening for sleeping problems may aid in the early detection of cognitive impairment and dementia. The early diagnosis of dementia has many important benefits, such as providing a patient the opportunity to more activity direct their future plans and health care decisions.

Prolonged Sleep May Predict Dementia Risk

Posted 6 days ago on Thursday, February 23rd, 2017 in Featured, Research


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Short Term Sleep Deprivation Affects Heart Function

Summary: A new study reports short term sleep deprivation in the context of 24 hour shifts can lead to an increase in blood pressure and heart rate.

Source: RSNA.

Too little sleep takes a toll on your heart, according to a new study to be presented today at the annual meeting of the Radiological Society of North America (RSNA).

People who work in fire and emergency medical services, medical residencies and other high-stress jobs are often called upon to work 24-hour shifts with little opportunity for sleep. While it is known that extreme fatigue can affect many physical, cognitive and emotional processes, this is the first study to examine how working a 24-hour shift specifically affects cardiac function.

“For the first time, we have shown that short-term sleep deprivation in the context of 24-hour shifts can lead to a significant increase in cardiac contractility, blood pressure and heart rate,” said study author Daniel Kuetting, M.D., from the Department of Diagnostic and Interventional Radiology at the University of Bonn in Bonn, Germany.

For the study, Dr. Kuetting and colleagues recruited 20 healthy radiologists, including 19 men and one woman, with a mean age of 31.6 years. Each of the study participants underwent cardiovascular magnetic resonance (CMR) imaging with strain analysis before and after a 24-hour shift with an average of three hours of sleep.

“Cardiac function in the context of sleep deprivation has not previously been investigated with CMR strain analysis, the most sensitive parameter of cardiac contractility,” Dr. Kuetting said.

The researchers also collected blood and urine samples from the participants and measured blood pressure and heart rate.

Following short-term sleep deprivation, the participants showed significant increases in mean peak systolic strain (pre = -21.9; post = -23.4), systolic (112.8; 118.5) and diastolic (62.9; 69.2) blood pressure and heart rate (63.0; 68.9). In addition, the participants had significant increases in levels of thyroid stimulating hormone (TSH), thyroid hormones FT3 and FT4, and cortisol, a hormone released by the body in response to stress.

Image shows an alarm clock.

Although the researchers were able to perform follow-up examinations on half of the participants after regular sleep, Dr. Kuetting notes that further study in a larger cohort is needed to determine possible long-term effects of sleep loss.

“The study was designed to investigate real-life work-related sleep deprivation,” Dr. Kuetting said. “While the participants were not permitted to consume caffeine or food and beverages containing theobromine, such as chocolate, nuts or tea, we did not take into account factors like individual stress level or environmental stimuli.”

As people continue to work longer hours or work at more than one job to make ends meet, it is critical to investigate the detrimental effects of too much work and not enough sleep. Dr. Kuetting believes the results of this pilot study are transferable to other professions in which long periods of uninterrupted labor are common.

“These findings may help us better understand how workload and shift duration affect public health,” he said.

ABOUT THIS SLEEP RESEARCH ARTICLE

Co-authors on the study are Andreas Feisst, M.D., Rami Homsi, M.D., Julian A. Luetkens, M.D., Daniel Thomas, M.D., Ph.D., Hans H. Schild, M.D., and Darius Dabir, M.D.

Source: Linda Brooks – RSNA
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will be presented at the RSNA 2016 – 102nd Scientific Assembly and Annual Meeting.

Loss of REM Sleep Linked to Desire For Fatty and Sugary Foods

Summary: A lack of REM sleep may lead to an increased desire to consume unhealthy foods, a new study reports.

Source: University of Tsukuba.

It is not well understood what role sleep loss plays in affecting areas of the brain that control the desire to consume unhealthy foods. A new paper published on December 6 in the journal eLife finds that rapid eye movement (REM) sleep loss leads to increased consumption of unhealthy foods, specifically sucrose and fat.

The researchers at the University of Tsukuba’s International Institute for Integrative Sleep Medicine (IIIS) used a new method to produce REM sleep loss in mice along with a chemical-genetic technique to block prefrontal cortex neurons and the behaviors they mediate. As a result, the IIIS researchers discovered that inhibiting these neurons reversed the effect of REM sleep loss on sucrose consumption while having no effect on fat consumption.

REM sleep is a unique phase of sleep in mammals that is closely associated with dreaming and characterized by random eye movement and almost complete paralysis of the body.

The prefrontal cortex plays a role in judging the palatability of foods through taste, smell and texture. Moreover, persons who are obese tend to have increased activity in the prefrontal cortex when exposed to high calorie foods.

Image shows a sleeping mouse dreaming about food.

“Our results suggest that the medial prefrontal cortex may play a direct role in controlling our desire to consume weight promoting foods, high in sucrose content, when we are lacking sleep,” says Kristopher McEown, the lead author on this project.

ABOUT THIS GENETICS RESEARCH ARTICLE

IIIS was launched by the Ministry of Education, Culture, Sports, Science and Technology of Japan with the aim of building globally visible research centers. At IIIS gather globally prominent scientists from multiple research fields contributing to elucidate the fundamental principles of sleep/wake regulation, and develop new strategies to assess and treat sleep diseases as well as the closely associated metabolic and mental disorders.

Funding: The research was funded by the Japan Society for the Promotion of Science.

Source: Masataka Sasabe – University of Tsukuba
Image Source: NeuroscienceNews.com image is credited to University of Tsukuba.
Original Research: Full open access research for “Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption” by Kristopher McEown, Yohko Takata, Yoan Cherasse, Nanae Nagata, Kosuke Aritake, and Michael Lazarus in eLife. Published online December 6 2016 doi:10.7554/eLife.20269

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Tsukuba. “Loss of REM Sleep Linked to Desire For Fatty and Sugary Foods.” NeuroscienceNews. NeuroscienceNews, 6 December 2016.
<http://neurosciencenews.com/sleep-loss-fatty-food-5693/&gt;.

Abstract

Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption

Rapid eye movement (REM) sleep loss is associated with increased consumption of weight-promoting foods. The prefrontal cortex (PFC) is thought to mediate reward anticipation. However, the precise role of the PFC in mediating reward responses to highly palatable foods (HPF) after REM sleep deprivation is unclear. We selectively reduced REM sleep in mice over a 25–48 hr period and chemogenetically inhibited the medial PFC (mPFC) by using an altered glutamate-gated and ivermectin-gated chloride channel that facilitated neuronal inhibition through hyperpolarizing infected neurons. HPF consumption was measured while the mPFC was inactivated and REM sleep loss was induced. We found that REM sleep loss increased HPF consumption compared to control animals. However, mPFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. Our findings provide, for the first time, a causal link between REM sleep, mPFC function and HPF consumption.

“Chemogenetic inhibition of the medial prefrontal cortex reverses the effects of REM sleep loss on sucrose consumption” by Kristopher McEown, Yohko Takata, Yoan Cherasse, Nanae Nagata, Kosuke Aritake, and Michael Lazarus in eLife. Published online December 6 2016 doi:10.7554/eLife.20269

Sleep Helps Process Traumatic Experiences

Summary: A new study reveals sleep could be used as an early prevention strategy against PTSD.

Source: University of Zurich.

If we sleep in the first 24 hours after a traumatic experience, this helps pigeonhole and process the distressing memories more effectively, as researchers from the University of Zurich and the Psychiatric University Hospital Zurich demonstrate in a new study. Sleep could thus be used as an early prevention strategy for posttraumatic stress disorders.

Does sleep help process stress and trauma? Or does it actually intensify emotional reactions and memories of the event? This previously unanswered question is highly relevant for the prevention of trauma-related disorders, such as posttraumatic stress disorder (PTSD). How extremely distressing experiences are processed right at the outset can influence the further course and development of posttraumatic stress disorders. PTSD patients experience highly emotional and distressing memories or even flashbacks where they feel as if they are experiencing their trauma all over again. Sleep could play a key role in processing what they have suffered.

A study conducted by a team from the Department of Psychology at the University of Zurich and the Psychiatric University Hospital Zurich has now tackled the question as to whether sleep during the first 24 hours after a trauma has a positive impact on highly emotional distress and memories related to traumatic events. In the lab, the researchers showed test subjects a traumatic video. The recurring memories of the images in the film that haunted the test subjects for a few days were recorded in detail in a diary. Virtually out of the blue, the test subjects would see a snapshot of what they had seen in their mind’s eye, reawakening the unpleasant feelings and thoughts they had experienced during the film. The quality of these memories resembles those of patients suffering from posttraumatic stress disorders. Other than after a traumatic event, however, they reliably disappear after a few days.

Fewer Distressing Emotional Memories

Study participants were randomly assigned to two groups. One slept in the lab for a night after the video while their sleep was recorded via an electroencephalograph (EEG); the other group remained awake. “Our results reveal that people who slept after the film had fewer and less distressing recurring emotional memories than those who were awake,” explains first author Birgit Kleim from the Department of Experimental Psychopathology and Psychotherapy at the University of Zurich. “This supports the assumption that sleep may have a protective effect in the aftermath of traumatic experiences.”

Image shows a woman sleeping.

On the one hand, sleep can help weaken emotions connected to an existing memory, such as fear caused by traumatic experiences, for instance. On the other hand, it also helps contextualize the recollections, process them informationally and store these memories. However, this process presumably takes several nights.

According to the authors of the study, recommendations on early treatments and dealing with traumatized people in the early phase are few and far between. “Our approach offers an important non-invasive alternative to the current attempts to erase traumatic memories or treat them with medication,” says Birgit Kleim. “The use of sleep might prove to be a suitable and natural early prevention strategy.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: University of Zurich
Image Source: NeuroscienceNews.com image is adapted from the University of Zurich press release.
Original Research: Abstract for “Effects of Sleep after Experimental Trauma on Intrusive Emotional Memories” by Birgit Kleim, PhD; Julia Wysokowsky, MSc; Nuria Schmid, MSc; Erich Seifritz, MD; and Björn Rasch, PhD in Sleep. Published online December 2016 doi:10.5665/sleep.6310

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Zurich. “Sleep Helps Process Traumatic Experiences.” NeuroscienceNews. NeuroscienceNews, 13 December 2016.
<http://neurosciencenews.com/sleep-trauma-psychology-5732/&gt;.

Abstract

Effects of Sleep after Experimental Trauma on Intrusive Emotional Memories

Study Objectives:

To investigate sleep’s effect in the immediate aftermath of experiencing an analog trauma in the laboratory on reducing intrusive emotional memory formation.

Methods:

Sixty-five healthy women were exposed to an experimental laboratory trauma. They viewed a neutral and a trauma film in the laboratory and were randomly allocated to either a group that slept following film viewing or a group that remained awake. Sleep was recorded with electroencephalogram in a subgroup of participants in the sleep group. All participants recorded intrusive memories in the week following the film.

Results:

The sleep group experienced fewer and less distressing intrusive trauma memories compared to the wake group. These effects were particularly evident toward the end of the week. Duration spent in stage N2 as opposed to light N1 sleep, a higher number of fast parietal sleep spindles and a lower rapid eye movement sleep density predicted intrusion frequency.

Conclusions:

Our results have clinical implications and set the ground for early-intervention sleep studies following trauma and prevention of chronic posttrauma disorders.

“Effects of Sleep after Experimental Trauma on Intrusive Emotional Memories” by Birgit Kleim, PhD; Julia Wysokowsky, MSc; Nuria Schmid, MSc; Erich Seifritz, MD; and Björn Rasch, PhD in Sleep. Published online December 2016 doi:10.5665/sleep.6310

Neurons Paralyze Us During REM Sleep

Summary: Researchers have identified a population of neurons that appear to be responsible for muscle paralysis during REM sleep.

Source: INSERM.

During REM sleep, the brain inhibits the motor system, which makes the sleeper completely immobile. CNRS researchers working in the Centre de Recherche en Neurosciences de Lyon (CNRS/Université Claude Bernard Lyon 1/INSERM/Université Jean Monnet) have identified a population of neurons that is responsible for this transient muscle paralysis. The animal model created will shed light on the origin of some paradoxical sleep disorders, and more particularly the condition that prevents this paralysis. It will also be most useful in the study of Parkinson’s disease, since these pathologies are related. This work was published on December 12, 2016 on the website of the journal Brain.

In spite of being in a deep sleep, the patients talk, move, kick and eventually fall out of bed. They are suffering from a parasomnia called REM Sleep Behavior Disorder (RBD). This disorder usually appears around the age of 50. Muscles are at rest during the REM sleep phase, but in these patients, there is no paralysis, although the reason for this is not known. The sleepers move abnormally, probably reflecting their dream activity.

A team from the Centre de Recherche en Neurosciences de Lyon has taken one more step towards elucidating this pathology. The researchers identified neurons in the sublaterodorsal nucleus of the brain, ideally located to control motor system paralysis during REM sleep. In rats, they specifically targeted this neuron population, by adding genetically modified viral vectors to it. Once these are in the neural cells, they block the expression of a gene that allows synaptic glutamate secretion. Now incapable of releasing this excitatory neurotransmitter, the neurons can no longer communicate with their neighbors. They are disconnected from the cerebral network necessary for paralysis during REM sleep.

For 50 years, the scientific community has considered that these glutamate neurons generated REM itself. This team’s experience invalidates this hypothesis: despite the absence of activity in this neuron circuit, the rats still experience this stage of sleep. They are fast asleep and disconnected from the outside world, with eyes closed. But these rats are no longer paralyzed. Their behavior is very reminiscent of the clinical profile of patients suffering from RBD. The glutamate neurons targeted in this study play an essential part in REM paralysis during sleep and are reportedly the first neurons affected in this neurological disease.

Image shows a brain slice with glutamate neurons.

This research work goes beyond creating a new preclinical model that mimics this parasomnia. It may be of paramount importance in studying some neurodegenerative diseases. Recent clinical research has shown that patients diagnosed with RBD almost always develop the motor symptoms of Parkinson’s disease, on average a decade later. The team is now attempting to develop an animal model that evolves from parasomnia into Parkinson’s disease, in order to understand how neuron degeneration occurs.

ABOUT THIS SLEEP RESEARCH ARTICLE

Source: INSERM
Image Source: NeuroscienceNews.com image is credited to Sara Valencia Garcia / Patrice Fort, CNRS.
Original Research: The study will appear in Brain.