Dream control study to further dream engineering for more creativity and how sounds may be incorporated

Amazing stuff! I don't believe we have made much progress on dream research since the days when individuals would lay down to tell Sigmund Freud what they dreamed about lately! 😊

"Researchers have shown they can achieve some control over what people are dreaming ...

researchers at Northwestern University (NU) were particularly interested in finding out if they could harness dreams to work with the idea that sleeping on a problem can help people solve it.

So they recruited 20 people who were experienced in lucid dreaming, the ability to recognize that you're dreaming from within a dream and sometimes control what happens. Another dream-related study released this month showed that lucid dreams might be able to help with mental health therapy for conditions like PTSD and Parkinson's disease, and previous work with researchers from NU and other institutes showed a simple type of communication was possible between lucid dreamers and test administrators. ..."

"... A new study by neuroscientists at Northwestern University validates the possibility of influencing dreams and offers a crucial step to support the theory that dreams in REM sleep — the rapid eye movement phase of sleep in which lucid dreaming can occur — may be especially conducive to helping individuals come up with creative solutions to a problem. ..."

From the abstract:

"Dreams have arguably been a source of creative insight for millennia. The specific assertion that dreams during rapid eye movement (REM) sleep promote creative problem-solving, however, has only anecdotal support, lacking strong empirical support from rigorous studies. Experimental manipulations of dream content have been confounded by waking components, such that any boost in creative problem-solving could be attributable to waking cognition rather than sleep cognition. Likewise, correlational evidence cannot unequivocally establish that dreams cause insights. Evidence that memory reactivation during sleep promotes creative problem-solving is also insufficient for implicating dreaming per se. Better methods for directly manipulating REM-sleep dreaming are needed. Here, we studied individuals who frequently have lucid dreams—realizing they are dreaming while still asleep. Participants slept after failing to solve several puzzles that had unique soundtracks, and they were instructed to continue working on a puzzle if they heard its soundtrack in a dream. Half of the soundtracks were played during REM sleep to reactivate memories of corresponding puzzles, with the goal of biasing dreams to connect with those specific puzzles versus the remaining puzzles. Those sound cues reliably increased dreaming about the associated puzzles. Furthermore, a post-hoc analysis showed that, for participants with an increase in cue-related dreaming, cues boosted later puzzle-solving. We thus expanded on a well-known phenomenon, that sounds can be incorporated into dreams and can change dream content, by substantiating experimental procedures to align dreams with the search for creative answers to specific challenges. Results highlight that REM dreams can contribute to next-day problem solving."

Dream control study turns sci-fi to science fact

Dream engineering can help solve ‘puzzling’ questions "Study offers insights to optimizing sleep for creativity"

Creative problem-solving after experimentally provoking dreams of unsolved puzzles during REM sleep (open access)

Fig. 1 Experimental timeline.

(A) Overview of experimental timeline for most participants.

(B) Each in-lab session had an identical procedure, except with different puzzles. Lucid dreams were induced with targeted lucidity reactivation (TLR).

One night of sleep vital signs may Predict Illness several years ahead and over 100 health conditions

Amazing stuff!

"Difficulty sleeping often precedes heart disease, psychiatric disorders, and many other illnesses. Researchers used data gathered during sleep studies to detect such conditions.

What’s new: SleepFM is a system that classifies Alzheimer’s, Parkinson’s, prostate cancer, stroke, congestive heart failure, and many other conditions based on a person’s vital signs while asleep — as much as 6 years before they show symptoms. ...

Input/output: Recordings of one night of sleep in, disease classifications out

Architecture: Convolutional neural network encoder, transformer, LSTM

Performance: Can accurately classify over 130 conditions ...

How it works: SleepFM comprises a convolutional neural network (CNN), transformer, and LSTM. The authors trained the system in two stages:

(i) to encode patterns in sleep data and

(ii) to classify diseases.

The training data comprised roughly 585,000 hours of sleep-study recordings that included, in addition to each patient’s age and sex, signals of activity in the brain, heart, respiratory system (airflow, snoring, and blood oxygen level), and leg muscles. The data was mostly proprietary but included public datasets.

The authors trained the CNN and transformer together.  ...

The authors added the LSTM and separately trained it, given 9 hours of sleep data as well as the subject’s age and sex, to classify more than 1,000 diseases.

Results: The authors compared SleepFM’s performance on a proprietary test set to the same system without pretraining and a vanilla neural network that was trained on only demographic information.

Across 14 general categories of disease ..."

From the abstract:

"Sleep is a fundamental biological process with broad implications for physical and mental health, yet its complex relationship with disease remains poorly understood. Polysomnography (PSG)—the gold standard for sleep analysis—captures rich physiological signals but is underutilized due to challenges in standardization, generalizability and multimodal integration.

To address these challenges, we developed SleepFM, a multimodal sleep foundation model trained with a new contrastive learning approach that accommodates multiple PSG configurations.

Trained on a curated dataset of over 585,000 hours of PSG recordings from approximately 65,000 participants across several cohorts, SleepFM produces latent sleep representations that capture the physiological and temporal structure of sleep and enable accurate prediction of future disease risk.

From one night of sleep, SleepFM accurately predicts 130 conditions with a C-Index of at least 0.75 (Bonferroni-corrected P < 0.01), including all-cause mortality (C-Index, 0.84), dementia (0.85), myocardial infarction (0.81), heart failure (0.80), chronic kidney disease (0.79), stroke (0.78) and atrial fibrillation (0.78).

Moreover, the model demonstrates strong transfer learning performance on a dataset from the Sleep Heart Health Study—a dataset that was excluded from pretraining—and performs competitively with specialized sleep-staging models such as U-Sleep and YASA on common sleep analysis tasks, achieving mean F1 scores of 0.70–0.78 for sleep staging and accuracies of 0.69 and 0.87 for classifying sleep apnea severity and presence.

This work shows that foundation models can learn the language of sleep from multimodal sleep recordings, enabling scalable, label-efficient analysis and disease prediction."

The New Open-Weights Leader, Big AI’s Political Influence, Predicting Illness, Faster Reasoning

New AI model predicts disease risk while you sleep "Stanford Medicine scientists and their colleagues created the first artificial intelligence model that can predict more than 100 health conditions from one night’s sleep."

A multimodal sleep foundation model for disease prediction (open access)

Fig. 1: Overview of SleepFM framework.

Jellyfish and sea anemones surprisingly sleep like humans to protect nerve cells

Amazing stuff!

"Turns out jellyfish and sea anemones – among the ancient creatures with a nervous system instead of a brain – have a very similar sleeping routine to our own. A new study published in Nature Communications reveals that these animals not only sleep but do so for the same portion of their day as humans, spending about one-third of the day sleeping. The findings also suggest that sleep evolved long before the brain to help maintain cells under stress. ..."

"... the most basic and ancient role of sleep is to protect nerve cells from cellular stress and the accumulation of DNA damage. ..."

From the abstract:

"Sleep is a conserved behavior across all animals with a nervous system, ranging from cnidarians to humans. Considering the survival risks, why sleep evolved in basal lineages and what essential benefits it provides to the simple nerve net of nocturnal and diurnal invertebrates remain elusive.

We used behavioral criteria to empirically define sleep in the upside-down jellyfish Cassiopea andromeda and the starlet sea anemone Nematostella vectensis.

Light and homeostasis were the primary drivers of sleep in C. andromeda, which slept at night and napped at midday in both the laboratory and the natural habitat. In contrast, both the circadian clock and homeostatic processes regulated sleep in N. vectensis, which increased sleep at dawn.

Similar to humans, C. andromeda, wild-type (WT) and Clock mutant (NvClkΔ/Δ) N. vectensis slept about one-third of the day, irrespective of the daily timing and architecture of sleep, and melatonin promoted sleep in accordance with the species-specific chronotype.

Notably, sleep deprivation, ultraviolet radiation, and mutagens increased neuronal DNA damage and sleep pressure, while spontaneous and induced sleep facilitated genome stability in both the diurnal and crepuscular cnidarians. These results suggest that DNA damage and cellular stress in simple nerve nets may have driven the evolution of sleep."

Jellyfish and sea anemones surprisingly sleep like humans

Why Do We Sleep at All? The Surprising Answer from the Sea (original news release) "Researchers at Bar-Ilan University decode an ancient sleep mechanism and reveal that sleep protects nerve cell."

DNA damage modulates sleep drive in basal cnidarians with divergent chronotypes (open access)

Fig. 1: Generalizing the characterization of sleep in C. andromeda across sizes and habitats.

Fig. 4: Sleep reduces DNA damage in neurons of cnidarians.

Stanford Researchers Build SleepFM Clinical: A Multimodal Sleep Foundation AI Model to accurately predict over 130 Disease conditions after one night of sleep

Amazing stuff! And this is only the beginning! We are deciphering the "language of sleep"!

Sweet dreams! 

"A team of Stanford Medicine researchers have introduced SleepFM Clinical, a multimodal sleep foundation model that learns from clinical polysomnography and predicts long term disease risk from a single night of sleep. ..."

"... SleepFM analyzed more than 1,000 disease categories in the health records and found 130 that could be predicted with reasonable accuracy by a patient’s sleep data. The model’s predictions were particularly strong for cancers, pregnancy complications, circulatory conditions and mental disorders, achieving a C-index higher than 0.8. ...

“We were pleasantly surprised that for a pretty diverse set of conditions, the model is able to make informative predictions,”  ..."

From the abstract:

"Sleep is a fundamental biological process with broad implications for physical and mental health, yet its complex relationship with disease remains poorly understood.

Polysomnography (PSG)—the gold standard for sleep analysis—captures rich physiological signals but is underutilized due to challenges in standardization, generalizability and multimodal integration.

To address these challenges, we developed SleepFM, a multimodal sleep foundation model trained with a new contrastive learning approach that accommodates multiple PSG configurations.

Trained on a curated dataset of over 585,000 hours of PSG recordings from approximately 65,000 participants across several cohorts, SleepFM produces latent sleep representations that capture the physiological and temporal structure of sleep and enable accurate prediction of future disease risk.

From one night of sleep, SleepFM accurately predicts 130 conditions with a C-Index of at least 0.75 (Bonferroni-corrected P < 0.01), including all-cause mortality (C-Index, 0.84), dementia (0.85), myocardial infarction (0.81), heart failure (0.80), chronic kidney disease (0.79), stroke (0.78) and atrial fibrillation (0.78).

Moreover, the model demonstrates strong transfer learning performance on a dataset from the Sleep Heart Health Study—a dataset that was excluded from pretraining—and performs competitively with specialized sleep-staging models such as U-Sleep and YASA on common sleep analysis tasks, achieving mean F1 scores of 0.70–0.78 for sleep staging and accuracies of 0.69 and 0.87 for classifying sleep apnea severity and presence.

This work shows that foundation models can learn the language of sleep from multimodal sleep recordings, enabling scalable, label-efficient analysis and disease prediction."

Stanford Researchers Build SleepFM Clinical: A Multimodal Sleep Foundation AI Model for 130+ Disease Prediction - MarkTechPost

New AI model predicts disease risk while you sleep (original news release) "Stanford Medicine scientists and their colleagues created the first artificial intelligence model that can predict more than 100 health conditions from one night’s sleep."

A multimodal sleep foundation model for disease prediction (open access)

Fig. 1: Overview of SleepFM framework.

Nighttime exposure to light while sleeping may raise cardiovascular risk by up to 50%

When sleeping, keep it dark!

"Exposure to light at night raises cardiovascular disease risk by up to 50 percent over sleeping in the dark, new research shows. But scientists say the effect isn’t from lack of sleep, but from disruption of the body’s master biological clock, the circadian rhythm. ...

For those experiencing the brightest nights, the research showed increased risk of between 30 percent and 50 percent for heart attack, stroke, heart failure, atrial fibrillation, and coronary artery disease. ...

The data did include light intensity but unfortunately provided no information about sources, such as streetlights, cellphone screens, nightlights, and television. ..."

From the key points and abstract:

"Key Points

Question  Is personal light exposure at night associated with cardiovascular disease incidence?

Findings  In this cohort study of 88 905 adults aged older than 40 years, exposure to brighter light at night was associated with higher risks of coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, and stroke, independent of established cardiovascular risk factors.

Meaning  These findings suggest that avoiding exposure to night light may lower risk of cardiovascular diseases.

Abstract

Importance  Light at night causes circadian disruption, which is a known risk factor for adverse cardiovascular outcomes. However, it is not well understood of cardiovascular diseases.

Objective  To assess whether day and night light exposure is associated with incidence of cardiovascular diseases, and whether associations of light with cardiovascular diseases differ according to genetic susceptibility, sex, and age.

Design, Setting, and Participants  This prospective cohort study analyzed cardiovascular disease records across 9.5 years (June 2013 to November 2022) from UK Biobank participants who wore light sensors in a naturalistic setting. Data were analyzed from September 2024 to July 2025.

Exposure  Approximately 13 million hours of light exposure data, tracked by wrist-worn light sensors (1 week each), categorized into the 0 to 50th, 51st to 70th, 71st to 90th, and 91st to 100th percentiles.

Main Outcomes and Measures

Incidence of coronary artery disease, myocardial infarction, heart failure, atrial fibrillation, and stroke after light tracking were derived from UK National Health Service records. Risks of cardiovascular diseases were assessed using Cox proportional hazards models (3 primary models adjusted at 3 levels) and reported as hazard ratios (HRs).

Results 

A total of 88 905 individuals were included (mean [SD] age, 62.4 [7.8] years; 50 577 female [56.9%]). Compared with individuals with dark nights (0-50th percentiles),

those with the brightest nights (91st-100th percentiles) had significantly higher risks of developing coronary artery disease (adjusted HR [aHR], 1.32; 95% CI, 1.18-1.46), myocardial infarction (aHR, 1.47; 95% CI, 1.26-1.71), heart failure (aHR, 1.56; 95% CI, 1.34-1.81), atrial fibrillation (aHR, 1.32; 95% CI, 1.18-1.46), and stroke (aHR, 1.28; 95% CI, 1.06-1.55).

These associations were robust after adjusting for established cardiovascular risk factors, including physical activity, smoking, alcohol, diet, sleep duration, socioeconomic status, and polygenic risk.

Larger-magnitude associations of night light with risks of heart failure (P for interaction = .006) and coronary artery disease (P for interaction = .02) were observed for females, and larger-magnitude associations of night light with risks of heart failure (P for interaction = .04) and atrial fibrillation (P for interaction = .02) were observed for younger individuals in this cohort.

Conclusions and Relevance

In this cohort study, night light exposure was a significant risk factor for developing cardiovascular diseases among adults older than 40 years. These findings suggest that, in addition to current preventive measures, avoiding light at night may be a useful strategy for reducing risks of cardiovascular diseases."

Nighttime exposure to light may raise cardiovascular risk by up to 50% — Harvard Gazette "New research suggests that it disrupts biological clock"

Light Exposure at Night and Cardiovascular Disease Incidence (open access)

The effects on the brain after sleep deprivation

Amazing stuff! The motto for today: Take care of your cerebrospinal fluid! This is my second blog post today covering cerebrospinal fluid (see here)!

"... A new study ... reveals what happens inside the brain as these momentary failures of attention occur. The scientists found that during these lapses, a wave of cerebrospinal fluid (CSF) flows out of the brain — a process that typically occurs during sleep and helps to wash away waste products that have built up during the day. This flushing is believed to be necessary for maintaining a healthy, normally functioning brain.

When a person is sleep-deprived, it appears that their body attempts to catch up on this cleansing process by initiating pulses of CSF flow. However, this comes at a cost of dramatically impaired attention. ..."

From the abstract:

"Sleep deprivation rapidly disrupts cognitive function and in the long term contributes to neurological disease. Why sleep deprivation has such profound effects on cognition is not well understood.

Here we use simultaneous fast fMRI–EEG to test how sleep deprivation modulates cognitive, neural and fluid dynamics in the human brain.

We demonstrate that attentional failures during wakefulness after sleep deprivation are tightly orchestrated in a series of brain–body changes, including neuronal shifts, pupil constriction and cerebrospinal fluid (CSF) flow pulsations, pointing to a coupled system of fluid dynamics and neuromodulatory state.

CSF flow and hemodynamics are coupled to attentional function within the awake state, with CSF pulsations following attentional impairment. The timing of these dynamics is consistent with a vascular mechanism regulated by neuromodulatory state.

The attentional costs of sleep deprivation may thus reflect an irrepressible need for rest periods driven by a central neuromodulatory system that regulates both neuronal and fluid physiology."

This is your brain without sleep | MIT News | Massachusetts Institute of Technology "New research shows attention lapses due to sleep deprivation coincide with a flushing of fluid from the brain — a process that normally occurs during sleep."

Attentional failures after sleep deprivation are locked to joint neurovascular, pupil and cerebrospinal fluid flow dynamics (open access)

Fig. 1: After sleep deprivation, CSF flow exhibits large sleep-like low-frequency waves during wakefulness.

When the human brain awakens after sleep

Amazing stuff!

"The process of transitioning from sleep to wakefulness (awakening) in humans has been shown to occur over several minutes. However, how the awakening process occurs at the level of brain activity remains to be fully elucidated.

Stephan et al. analyzed more than 1000 awakening events in humans using high-density electroencephalography (EEG) and revealed distinct spatiotemporal EEG signatures associated with awakening from non–rapid eye movement (non-REM) and REM sleep.

When present before waking up from non-REM sleep, this distinct EEG pattern was associated with feeling less sleepy. These results might have implications for sleep disorders associated with abnormal sleepiness during wakefulness."

From the highlights and abstract:

"Highlights

• High-density EEG reveals consistent cortical activation patterns upon awakening

• High-frequency arousal changes follow a front-to-back gradient across sleep stages

• Low-frequency arousal changes in NREM sleep start in a posterior-medial hotspot

• Different slow wave types show opposite relation to sleepiness upon awakening

Summary

How does the brain awaken from sleep? Several studies have suggested that the awakening process occurs asynchronously across brain regions, but the precise nature of these changes and how they are reflected in human electroencephalography (EEG) remains unknown.

Here, we recorded 1,073 awakenings and arousals with high-density EEG and mapped brain activity at a second-to-second timescale around movement onset using source modeling.

We found that cortical activity upon awakening progressed along highly consistent spatial and frequency gradients.

In awakenings and arousals from non-rapid eye movement (NREM) sleep, transient increases in low-frequency power preceded increases in high-frequency power by a few seconds,

whereas awakenings from REM sleep were mainly characterized by increases in high-frequency power.

Regardless of sleep stage, high-frequency changes were first seen in frontal and last in occipital and inferior-temporal cortical areas, whereas low-frequency changes in NREM sleep started in a centro-parietal “hotspot,” progressed frontally, and reached occipital and inferior-temporal regions last.

Finally, the presence of these spatio-temporal arousal patterns during sleep, before participants were awakened by sounds, was followed by lower sleepiness ratings upon awakening.

These results indicate a consistent spatio-temporal EEG signature of the awakening process that likely reflects the structural organization of arousal systems.

Importantly, a transient increase in slow EEG frequencies, which are normally associated with sleep, is inherent to the arousal process and functionally correlates with feeling more awake when awakening from NREM sleep.

These findings have important implications for the interpretation of arousal signals and the detection of incomplete awakenings in sleep disorders."

In Other Journals | Science

Cortical activity upon awakening from sleep reveals consistent spatio-temporal gradients across sleep stages in human EEG (open access)

Graphical abstract

New Brain Circuit Helps Recover Lost Sleep

Amazing stuff! When will be able to optimize our sleep for best performance and health? Don't hold your breath! 😊

"... Now, researchers ... identified a subgroup of neurons in the thalamus of the mouse brain are crucial for the homeostatic regulation of sleep, providing insights into how animals recover from lost sleep. ...

Curious to learn more about the neurons that regulate sleep, the researchers first mapped neural circuits upstream of known sleep-promoting brain regions in mice. After identifying 11 candidate regions, they injected mice with clozapine N-oxide, a synthetic molecule, to see if chemical activation of the excitatory neurons in those areas promoted sleep. Of these, the activation of a subset of excitatory neurons in the medial thalamic nucleus reuniens (mRE) led to the greatest increase in [non] REM sleep. ...

To further characterize these mRE neurons, the researchers employed chemogenetic and optogenetic tools. Using either method, they found that stimulated neurons led to mice that exhibited deeper and more prolonged NREM sleep several hours later. This suggested that these neurons do not directly induce sleep but instead regulate sleep homeostasis. The researchers also saw that when they activated mRE neurons with light, the mice engaged in enhanced typical pre-sleep behaviors, such as preparing a spot to sleep (nesting) or self-grooming. ..."

From the abstract of the perspective:

"Most animals regularly undergo an astonishing transformation by cycling between wakefulness and sleep. However, if sleep is disrupted or delayed, sleep “debt” accrues, resulting in longer and deeper sleep. Since the discovery of wake-promoting neurons in the brainstem in the 1940s, a hunt for the control mechanisms of sleep-wake behavior has led to a model of reciprocally connected wake-promoting and sleep promoting cell groups [or nuclei (1, 2)] that achieve discrete brain vigilance states by mutually inhibiting one another (3).

But how sleep loss results in rebound sleep to reestablish homeostasis has remained a mystery. On page 1291 of this issue, Lee et al. (4) report a group of neurons in the thalamus (the brain region that relays incoming sensory information to the cerebral cortex) that increases its activity during sleep deprivation and promotes sleep recovery and depth. The findings suggest that these neurons are responsible for promoting sleep homeostasis."

From the editor's summary and abstract:

"Editor’s summary

Sleep is tightly regulated by homeostatic forces, and sleep deficit leads to persistent and consolidated recovery sleep. However, the pathways underlying the homeostatic control of sleep are still unknown. Lee et al. now describe the first homeostatic sleep circuit in mammals (see the Perspective by Gilette and Lipton). This circuit comprises a cluster of excitatory neurons in the nucleus reuniens that is activated by sleep need and is necessary for recovery sleep. Stimulation of these neurons first triggers presleep behavior, followed by deep and persistent sleep that can last hours. This sleep pattern resembles recovery sleep and suggests that activation of reuniens neurons generates sleep pressure even in animals without sleep debt. Silencing this circuit during sleep deprivation disrupts the amount and quality of recovery sleep, suggesting that its activity signals the accrual of sleep need. ...

Structured Abstract

INTRODUCTION

Sleep is under homeostatic control: After prolonged wakefulness, animals engage in persistent, consolidated, and deep sleep. Although the homeostatic regulation of sleep has been intensely studied over the past century, the biological underpinnings of this process remain enigmatic. Progress is being made delineating molecular pathways that mediate sleep homeostasis. By contrast, the identity of neural circuits that sense and/or transmit homeostatic sleep signals is unclear.

RATIONALE

Sleep can be divided into rapid eye movement (REM) and non-REM (NREM) sleep, which is considered the deeper, more restorative form of sleep. To date, many NREM-promoting neural circuits have been identified. However, the identity of specific neuronal clusters required for the accrual of sleep need remains unclear, and the goal of this study was to identify such a neural circuit.

RESULTS

From a circuit screen in mice, a group of excitatory neurons in the thalamic nucleus reuniens (RE) was identified that projected to multiple downstream NREM-promoting clusters.

Brief optogenetic activation of RE neurons led to an unusual phenotype—persistent, consolidated, and deep NREM sleep after a delay. Notably, during this delay period before falling asleep, the animals engaged in sleep-preparatory behaviors, which included grooming and nesting.

Because the persistent, consolidated, and deep sleep phenotype resembled the homeostatic recovery sleep seen after sleep deprivation, we sought to investigate whether RE neurons participate in the homeostatic regulation of sleep.

Most NREM-promoting neurons exhibit increased activity during NREM sleep. To measure the in vivo activity of RE neurons, chronic Neuropixels recordings were performed during sleep deprivation and recovery sleep.

These recordings revealed that RE activity was greater during sleep deprivation and/or wakefulness and reduced during recovery sleep.

Next, we examined whether this elevated RE activity during sleep deprivation was necessary for the accrual of sleep need.

Chemogenetic inhibition of RE neurons during sleep deprivation decreased subsequent homeostatic recovery sleep amount, consolidation, and depth.

RE neurons promote NREM sleep by signaling to a previously identified NREM-promoting cluster in the zona incerta (ZI).

Unexpectedly, sleep deprivation induced neural plastic changes of the RE-ZI connection. The degree of this RE-ZI plasticity correlated with the amount of subsequent homeostatic recovery sleep.

Moreover, this synaptic plasticity enhanced the morphological and functional connectivity between the RE and ZI neuronal clusters.

Calcium- and calmodulin-dependent protein kinase II (CaMKII) is well described to regulate synaptic plasticity and has been implicated in the homeostatic regulation of sleep.

Inhibition of CaMKII activity in RE neurons reduced the RE-ZI plasticity and subsequent homeostatic recovery sleep triggered by sleep deprivation.

CONCLUSION

Our findings suggest that RE neurons are required for the accrual of sleep need and are able to generate persistent, deep sleep, similar to homeostatic recovery sleep.

Sleep deprivation induces plasticity of the RE-ZI circuit, strengthening the connectivity of this sleep-promoting module. The degree of this plasticity correlates with the amount of homeostatic sleep rebound, which suggests that RE-ZI plasticity serves as a molecular readout for sleep need.

These findings reveal a mechanism by which sleep loss transforms the functional coupling of a sleep circuit to promote persistent, deep sleep."

New Brain Circuit Helps Recover Lost Sleep | The Scientist "How do animals bounce back from sleep deprivation? Scientists found a subset of neurons in the mouse thalamus that repay this “sleep debt.”"

Where the brain pays sleep debt (no public access) "Neurons in the thalamus drive restorative sleep"

Sleep need–dependent plasticity of a thalamic circuit promotes homeostatic recovery sleep (no public access)

Sleep need–dependent plasticity of an RE-ZI circuit promotes homeostatic recovery sleep.

European Birds (crows) trade vigilance for rest while sleeping by keeping one eye less open

Amazing stuff! My conclusion: Smart birds need less vigilance! 😊

However, the scientists appear to have failed to document or mention where the research subjects ( were taken from or located (e.g. natural habitat, laboratory, urban area). This is quite an omission, so bad an omission that it may qualify as junk science. The researchers only mention "European jackdaws". The official news release by the Max Planck Neuroscience institute also does not mention at all where these "European jackdraws" came from.

I believe, it is critically important to mention where (in which environment) these birds were investigated. For example, I would argue that birds in urban areas may need to be less vigilant because there is an overpopulation of birds and fewer predators.

Caveat: I did read the entire article.

"Birds exhibit two types of non-REM sleep: 

symmetric (both brain hemispheres sleeping deeply) and 

asymmetric (one hemisphere sleeping lightly while the other stays alert). 

van Hasselt et al. investigated how birds balance these sleep modes under increased sleep pressure caused by deprivation.

Using high-density EEG on European jackdaws, researchers found that during heightened sleep need, birds prioritize symmetric sleep over asymmetric sleep, sacrificing vigilance to recover from sleep loss. This trade-off highlights the constraints imposed by the need for deep, restorative sleep on the birds’ ability to remain alert for potential threats."

"Summary:

• Birds, unlike humans, can sleep deeply with both halves of their brains (symmetrically) or with one half sleeping lighter than the other (asymmetrically).
• Study of European jackdaws led by an international team of researchers shows that when sleep-deprived, jackdaws were more likely to fall into deep sleep with both brain halves at the expense of keeping one half vigilant – especially early in the night, when the need to recover is greatest.
• Observing how birds navigate the trade-off between vigilance and sleep may help scientists better understand how sleep loss affects brain function more broadly, including in us.

... When humans sleep, our brains cycle through stages, alternating between rapid eye movement (REM) sleep and non-REM sleep roughly every 90 minutes. Birds go through these same stages, but typically in much shorter bursts – and their sleep patterns are far more flexible than ours. ..."

From the highlights and abstract:

"Highlights

• High-density EEG shows local homeostatic responses to sleep loss in the avian brain

• Theta oscillations occur during non-REM sleep in non-hippocampal brain regions

• Non-REM sleep occurs symmetrically and asymmetrically between the hemispheres

• Asymmetric sleep is sacrificed for symmetric sleep when sleep pressure increases

Summary

Sleep is a dangerous part of an animal’s life. Nonetheless, following sleep loss, mammals and birds sleep longer and deeper, as reflected by increased electroencephalogram (EEG) slow-wave activity (SWA; ≈1–5 Hz spectral power) during non-rapid eye movement (NREM) sleep.

Stimulating a brain region during wakefulness also causes that region to sleep deeper afterwards, indicating that NREM sleep is a local, homeostatically regulated process. 

Birds and some marine mammals can keep one eye open during NREM sleep, a behavior associated with lighter sleep or wakefulness in the hemisphere opposite the open eye—states called asymmetric and unihemispheric NREM sleep, respectively.

Closure of both eyes is associated with symmetric NREM or REM sleep.

Birds rely on asymmetric and unihemispheric sleep to stay safe. However, as sleeping deeply with only one hemisphere at a time increases the time required for both hemispheres to fulfill their need for NREM sleep, increased sleep pressure might cause birds to engage in symmetric sleep at the expense of asymmetric sleep. Using high-density EEG recordings of European jackdaws (Coloeus monedula), we investigated intra- and inter-hemispheric asymmetries during normal sleep and following sleep deprivation (SD). The proportion of asymmetric sleep was lower early in the sleep period and following SD—periods of increased sleep pressure. Our findings demonstrate a trade-off between the benefits of sleep and vigilance and indicate that a bird’s utilization of asymmetric sleep is constrained by temporal dynamics in their need for sleep."

In Other Journals | Science

Too tired to stay alert? A difficult trade-off between sleep and vigilance (original press release) "Sleep-deprived European jackdaws trade vigilance for deep sleep – a strategy that could carry risks in the wild."

Sleep pressure causes birds to trade asymmetric sleep for symmetric sleep

(open access)

Graphical abstract

Poor sleep throws your whole body out of whack, it is a metabolic disorder

Amazing stuff! Poor sleep or sleep loss is perhaps worse for your health than you thought! It is diabolic!

"... There are a million reasons why we don’t get as much sleep as we should. And that’s not just making us tired—it’s making us ill ... “Sleep loss can be aptly defined as a metabolic disorder,” ...

“ With wakefulness, we are creating all sorts of metabolic waste,” ... “And then when we sleep, we know that we are able to clear some of that cellular metabolite waste that we have generated throughout the day.” ...

outline all sorts of additional ways that cells behave differently on too little sleep, many of which impair the production of cellular fuel. “What we are trying to highlight is, truly, how profound those changes are in the cells of our body and brain,” ... “ to the point that perhaps we shouldn’t dismiss our sleep so easily.”"

From the abstract:

"Sleep loss dysregulates cellular metabolism and energy homeostasis. Highly metabolically active cells, such as neurons, enter a catabolic state during periods of sleep loss, which consequently disrupts physiological functioning.

Specific to the central nervous system, sleep loss results in impaired synaptogenesis and long-term memory, effects that are also characteristic of neurodegenerative diseases.

In this review, we describe how sleep deprivation increases resting energy expenditure, leading to the development of a negative energy balance—a state with insufficient metabolic resources to support energy expenditure—in highly active cells like neurons.

This disruption of energetic homeostasis alters the balance of metabolites, including adenosine, lactate, and lipid peroxides, such that energetically costly processes, such as synapse formation, are attenuated. During sleep loss, metabolically active cells shunt energetic resources away from those processes that are not acutely essential, like memory formation, to support cell survival. Ultimately, these findings characterize sleep loss as a metabolic disorder."

ScienceAdviser

Sleep loss is a metabolic disorder (a review, no public access)

Children’s mattresses and bedroom air can contain/emit toxic chemicals linked with developmental and hormonal disorders

Serious stuff! Concerning, almost shocking! Should this not have been discovered several decades ago? Some of the findings are disturbing e.g. violating existing rules.

Are e.g. flame retardants necessary in children's mattresses and how much of it?

"Children’s mattresses can emit toxic chemicals linked with developmental and hormonal disorders, two new studies have found; high levels of chemicals like phthalates and flame retardants were found near children’s beds, found a study published in Environmental Science & Technology, and a companion study identified mattresses as a key source of exposure. CNN"

From the abstract (1):

"Sleeping microenvironments (SMEs) can expose young children to chemicals of concern.

Using passive samplers, we measured the concentrations of ortho-phthalates (PAEs), organophosphate esters (OPEs), and UV-filters (benzophenones, salicylates, and phenolic benzotriazoles) in the bedroom air, SME, and released from mattresses in 25 bedrooms of children aged 6 months to 4 years in Toronto and Ottawa, Canada.

We detected 28, 31, and 30 compounds in bedroom air, SME air, and mattresses, respectively. SME exceeded bedroom air concentrations, indicating elevated exposure while sleeping and sources from SME contents, with two exceptions.

Higher concentrations of two PAEs and five OPEs (including isomers) in mattress versus SME samplers indicated that mattresses were a source.

Bedding items were likely sources of tris(2-butoxyethyl) phosphate (TBOEP) where SME concentrations were significantly higher than those in mattress samplers.

Older mattresses had higher concentrations of di-2-ethylhexyl phthalate (DEHP) and benzyl butyl phthalate (BzBP).

These results indicate children’s exposure to a range of chemicals of concern while sleeping, at higher concentrations than in their bedrooms.

Practical steps to reduce exposure include limiting items in SMEs such as toys and frequently washing bedding. Also, these results should prompt stricter regulations and greater producer responsibility regarding harmful chemicals used in mattresses and SME articles."

From the abstract (2):

"Our research found that children aged 1–4 years are being exposed to elevated levels of semivolatile organic compounds (SVOCs) in their sleeping microenvironment (SME).

We detected 21 SVOCs in four classes

(ortho-phthalates, 

organophosphate esters, 

benzophenones, and 

salicylates) in 16 new children’s mattresses. 

One mattress exceeded the Canadian regulatory limit of 0.1% (by weight) for children’s mattresses for di-n-butyl phthalate (DnBP), while five had >0.1% diisobutyl phthalate (DiBP), di-n-octyl phthalate (DnOP), and diisononyl phthalate (DiNP), which are regulated in children’s toys but not in mattresses. 

One mattress contained high levels of tris(2-chloroethyl) phosphate (TCEP), which has been prohibited from use in Canada since 2014.

Five mattresses had from 1 to 3% of several organophosphate esters.

No consistent trend was found between the number or concentrations of SVOCs in mattress covers and their polymer type, e.g., rigid polyvinyl chloride vs flexible polypropylene-polyethylene, identified using Fourier transform infrared spectroscopy (FTIR).

Twelve out of 45 SVOCs measured were emitted from eight mattresses tested at room temperature, rising to 20 detected at body temperature, and 21 were detected at body temperature and when body weight was applied.

Given the likelihood of exposure, these results show the need for stricter regulations of all harmful chemicals in children’s mattresses and improved oversight by manufacturers to minimize the use of harmful chemicals, especially when they are not needed."

Global Health NOW: Pandemic Agreement Reached; A Brain Bank Hangs in the Balance; and Spore-Driven Threats

Young Children’s Exposure to Chemicals of Concern in Their Sleeping Environment: An In-Home Study (study no. 1, open access)

Are Sleeping Children Exposed to Plasticizers, Flame Retardants, and UV-Filters from Their Mattresses? (study no. 2, open access)

Graphical abstract (1)

Graphical abstract (2)

ALS Disturbs Sleep Prior to onset of ALS Symptoms and associated genetic mutations

This seems to be a plausible connection! Do not older people get less sleep and sometimes less quality sleep (e.g. reduced rapid eye movement or REM)?

Unfortunately, the study did not investigate whether sleep disturbances cause ALS. We are left with a kind of a chicken and egg problem.

Therefore, I also suspect, the pre onset sleep disturbances are not a good indicator for developing ALS.

This mix of sleep disturbances and genetic mutations make this study confusing. More research is probably needed.

"Sleep disturbances are commonly reported by people with neurodegenerative conditions that damage motor neurons. Some of these disorders, including amyotrophic lateral sclerosis (ALS), affect nonmotor functions of the brain, including sleep, which is regulated by the hypothalamus. ...

The researchers started by investigating differences in sleep quality between individuals who had early-stage ALS, a period before the onset of respiratory problems, and people without ALS or other motor deficits. They observed that people with ALS took longer to fall asleep and had increased bouts of wake and rapid eye movement (REM) sleep but reduced deep sleep non-REM (NREM) stages.

In a second cohort of individuals with an immediate relation to someone with ALS but who had not developed motor symptoms, the researchers recorded their sleep and collected DNA samples to determine which individuals carried a genetic mutation associated with ALS.

Compared to individuals with no ALS mutations, presymptomatic ALS carriers demonstrated altered sleep patterns that were dependent on the mutation that they carried: 

one mutation was associated with less overall time asleep and reduced deep sleep NREM, while a 

second mutation led to a longer time to fall asleep and more time in REM, but less time in total in NREM stages. Both mutations were associated with increased times in the wake period. ...

The team confirmed the sleep changes they saw in their human studies using three different animal models of ALS with mutations in either an RNA-binding protein, a DNA-binding protein, or superoxide dismutase, all shown to be affected in the disorder. Although the onset of sleeping changes varied by genetic mutation, the researchers saw an overall decrease in NREM and REM and increased wake periods in animals; these changes occurred prior to motor deficits in one model. Thus, although the effects to REM sleep differed between mice and humans, ALS caused similar changes to sleep-wake patterns in both species. ..."

From the editor's note and abstract:

"Editor’s summary

Patients with amyotrophic lateral sclerosis (ALS) often experience poor sleep, but whether these disturbances are caused by alterations in sleep regulating brain circuits or triggered by motor symptoms remains unclear.

Guillot et al. found that patients with ALS and presymptomatic carriers of ALS risk genes show increased wakefulness and reduced non–rapid eye movement sleep. Disruptions in sleep architecture were also found in three mouse models of ALS and partially normalized by intraventricular injection of melanin-concentrating hormone or oral administration of an orexin antagonist.

These results suggest that sleep disturbances occur before symptom onset and can be ameliorated by targeting neuropeptides involved in sleep/wake regulation. ...

Abstract

Sleep alterations have been described in several neurodegenerative diseases yet are currently poorly characterized in amyotrophic lateral sclerosis (ALS).

This study investigates sleep macroarchitecture and related hypothalamic signaling disruptions in ALS. Using polysomnography, we found that both patients with ALS as well as asymptomatic C9ORF72 and SOD1 mutation carriers exhibited increased wakefulness and reduced non–rapid eye movement sleep.

Increased wakefulness correlated with diminished cognitive performance in both clinical cohorts. Similar changes in sleep macroarchitecture were observed in three ALS mouse models (Sod1G86R, FusΔNLS/+, and TDP43Q331K).

A single oral administration of a dual-orexin receptor antagonist or intracerebroventricular delivery of melanin-concentrating hormone (MCH) through an osmotic pump over 15 days partially normalized sleep patterns in mouse models. MCH treatment did not extend the survival of Sod1G86R mice but did decrease the loss of lumbar motor neurons. These findings suggest MCH and orexin signaling as potential targets to treat sleep alterations that arise in early stages of the disease."

ALS Disturbs Sleep Prior to Symptom Onset | The Scientist "Humans and mice with a predisposition for ALS displayed altered sleep patterns before symptoms began, offering a potential novel diagnostic and treatment approach."

Early-onset sleep alterations found in patients with amyotrophic lateral sclerosis are ameliorated by orexin antagonist in mouse models (no public access)

All exercise improves insomnia, but muscle exercises are better than others

Strengthen your muscles for better sleep! More weight lifting before sleep!

I get already sleepy just thinking about exercise! 😊

"... The study was a systematic review and meta-analysis of 25 randomized controlled trials conducted between 1996 and 2021, encompassing 2,170 participants. It evaluated and compared the impact of different types of physical exercise on sleep quality in adults aged 60 and older. Participants were included if they had been diagnosed with insomnia according to DSM-5 criteria. ...

The exercise type that produced the best effect on sleep quality was strength or resistance training. This includes using free weights, weight machines or resistance bands. ..."

From the abstract:

"Abstract

Objective

To measure the impact of each type of exercise on sleep quality and identify the exercise that enhances sleep quality the most.

Study selection

Eligible randomised controlled trials that compare physical exercise to routine activities, usual care, non-physical activity, or health education to measure the Pittsburgh Sleep Quality Index.

Data source

Studies retrieved from Medline, Embase, CINAHL, Scopus, ClinicalTrial.gov and ThaiJo from the database’s inception to October 2022.

Data extraction and synthesis

Two reviewers independently identified studies, collected data and assessed bias. In the absence of heterogeneity, a fixed effect model was used for pairwise meta-analysis. Alternatively, a random effect model was used. A two-stage network meta-analysis used the surface under the cumulative ranking curve (SUCRA) to compare exercise efficacy.

Main outcome

Global Pittsburgh Sleep Quality Index (GPSQI) and subdomain score.

Results

This review comprised 2170 people from 25 trials. Direct meta-analysis revealed significant improvement in GPSQI with combined exercise (unstandardised mean difference (USMD) −2.35, 95% CI−3.13 to –1.57, p<0.001, I2=69.13%). GPSQI decreased considerably with aerobic activity (USMD −4.36, 95% CI −7.86 to –0.86, p=0.01, I2=97.83%). For the network meta-analysis, strengthening, aerobic and combination exercise significantly lowered GPSQI (USMD−5.75, –3.76 and −2.54, respectively). Strength training improved GPSQI scores most effectively (SUCRA 94.6%).

Conclusion

Exercise that strengthens muscles, rather than aerobic or combination exercises, is the most effective way to enhance sleep quality."

All exercise improves insomnia, but some types are better than others "A new study has ranked the best types of exercise for improving sleep quality. The findings demonstrate that exercise is an easy-to-implement, relatively cheap, and particularly effective way of treating insomnia, a common problem for older adults."

Impact of different types of physical exercise on sleep quality in older population with insomnia: a systematic review and network meta-analysis of randomised controlled trials (open access)

Pupil size in sleep reveals how memories are processed

Amazing stuff! More on the enigma of longer term memory formation!

"The eyes may be the window to the soul, but the pupil is key to understanding how, and when, the brain forms strong, long-lasting memories ...

By studying mice equipped with brain electrodes and tiny eye-tracking cameras, the researchers determined that new memories are being replayed and consolidated when the pupil is contracted during a substage of non-REM sleep.

When the pupil is dilated, the process repeats for older memories. The brain’s ability to separate these two substages of sleep with a previously unknown micro-structure is what prevents “catastrophic forgetting” in which the consolidation of one memory wipes out another one.  ...

The recordings showed that the temporal structure of sleeping mice is more varied, and more akin to the sleep stages in humans, than previously thought.

By interrupting the mice’s sleep at different moments and later testing how well they recalled their learned tasks, the researchers were able to parse the processes. When a mouse enters a substage of non-REM sleep, its pupil shrinks, and it’s here the recently learned tasks – i.e., the new memories – are being reactivated and consolidated while previous knowledge is not. Conversely, older memories are replayed and integrated when the pupil is dilated. ..."

From the abstract:

"Recently acquired memories are reactivated in the hippocampus during sleep, an initial step for their consolidation. This process is concomitant with the hippocampal reactivation of previous memories posing the problem of how to prevent interference between older and recent, initially labile, memory traces. Theoretical work has suggested that consolidating multiple memories while minimizing interference can be achieved by randomly interleaving their reactivation.

An alternative is that a temporal microstructure of sleep can promote the reactivation of different types of memories during specific substates.

Here, to test these two hypotheses, we developed a method to simultaneously record large hippocampal ensembles and monitor sleep dynamics through pupillometry in naturally sleeping mice. Oscillatory pupil fluctuations revealed a previously unknown microstructure of non-REM sleep-associated memory processes. We found that memory replay of recent experiences dominated in sharp-wave ripples during contracted pupil substates of non-REM sleep, whereas replay of previous memories preferentially occurred during dilated pupil substates. Selective closed-loop disruption of sharp-wave ripples during contracted pupil non-REM sleep impaired the recall of recent memories, whereas the same manipulation during dilated pupil substates had no behavioural effect. Stronger extrinsic excitatory inputs characterized the contracted pupil substate, whereas higher recruitment of local inhibition was prominent during dilated pupil substates. Thus, the microstructure of non-REM sleep organizes memory replay, with previous versus new memories being temporally segregated in different substates and supported by local and input-driven mechanisms, respectively. Our results suggest that the brain can multiplex distinct cognitive processes during sleep to facilitate continuous learning without interference."

Pupil size in sleep reveals how memories are processed "Cornell University researchers have found that the pupil is key to understanding how, and when, the brain forms strong, long-lasting memories."

Pupil size in sleep reveals how memories are sorted and preserved (original news release)

Sleep microstructure organizes memory replay (no public access)

Sleep resets neurons for new memories the next day

Amazing stuff! Solving the mysteries of human memory.

"... The hippocampus is divided into three regions: CA1, CA2 and CA3. CA1 and CA3 are involved in encoding memories related to time and space and, are well-studied; less is known about CA2, which the current study found generates this silencing and resetting of the hippocampus during sleep. ..."

From the Perspective abstract:

"Sleep is not just a time for the body to rest but also for the mind to solidify memories. During the non-rapid eye movement (NREM) phase of sleep, neurons in the hippocampus display short bursts of firing activity called sharp-wave ripples (SWRs), which is essential for memory consolidation. How the brain rebalances its activity after these bursts remains unclear. ... Karaba et al. ... report a new type of neuron activity in the rodent hippocampus that is characterized by long episodes of neuronal firing called barrage of action potentials (BARR). BARRs counteract SWRs to suppress the increased activity of neurons involved in learning during NREM sleep. The findings demonstrate that BARRs are crucial for memory consolidation by modulating memory reactivation and help to reconcile different theories on the role of sleep for memory formation."

From the editor's summary and abstract:

"Editor’s summary

During sleep, there is an increase in the coordinated firing of neuronal ensembles that were previously active during behavior. These hippocampal sharp-wave ripples are necessary for sleep-dependent memory consolidation. However, how the hippocampus regulates such increases in ensemble reactivation and synchrony while keeping the overall homeostatic balance of the network is not known. Karaba et al. discovered a new type of network pattern, a barrage of activity, that originated in hippocampal area CA2 and involved pyramidal cells and a specific type of interneurons. This barrage had differential effects on the efferent CA1 neurons and was dependent on experience. Optogenetic manipulations of this activity indicated its role in different tasks. Unlike sharp-wave ripples, which increase hippocampal output, this barrage decreased the output, thereby rebalancing the network.

Abstract

Memory consolidation involves the synchronous reactivation of hippocampal cells active during recent experience in sleep sharp-wave ripples (SWRs). How this increase in firing rates and synchrony after learning is counterbalanced to preserve network stability is not understood. We discovered a network event generated by an intrahippocampal circuit formed by a subset of CA2 pyramidal cells to cholecystokinin-expressing (CCK+) basket cells, which fire a barrage of action potentials (“BARR”) during non–rapid eye movement sleep. CA1 neurons and assemblies that increased their activity during learning were reactivated during SWRs but inhibited during BARRs. The initial increase in reactivation during SWRs returned to baseline through sleep. This trend was abolished by silencing CCK+ basket cells during BARRs, resulting in higher synchrony of CA1 assemblies and impaired memory consolidation."

Sleep resets neurons for new memories the next day | Cornell Chronicle

A BARRage of firing while asleep (no public access)

A hippocampal circuit mechanism to balance memory reactivation during sleep (no public access)

Compensatory sleep can make up for sleep deprivation to reduce heart disease risk

Good news! If I remember correctly, then it was previously believed this was not possible!

"Sleep-deprived people who catch up on sleep over weekends may reduce their heart disease risk by a fifth, according to a British study of 90,000 people presented at the European Society of Cardiology Congress ..."

Global Health NOW: Rising Vax Misinformation; Mosquitoes Don’t Care About Political Boundaries; and The Real HouseWolves of Beverly Hills

Exploring cardiovascular health: lifestyle, economics, and disparities "Weekend compensatory sleep is associated with reduced risk of heart disease: a prospective UK Biobank-based cohort study"

Our brains take micro naps while we're awake – and micro wakes when we're asleep

Amazing stuff! There is more to sleep/wake than the long known "slow, long-lasting waves"!

"For the first time, scientists have discovered that a small region of our brain shuts down to take microsecond-long naps while we're awake. What's more, these same areas 'flicker' awake while we're asleep. These new findings could offer pivotal insights into neurodevelopmental and neurodegenerative diseases, which are linked to sleep dysregulation. ..."

"... For the first time, scientists have found that sleep can be detected by patterns of neuronal activity just milliseconds long, 1000 times shorter than a second, revealing a new way to study and understand the basic brain wave patterns that govern consciousness. They also show that small regions of the brain can momentarily “flicker” awake while the rest of the brain remains asleep, and vice versa from wake to sleep. ...

Over four years of work, Parks and Schneider trained a neural network to study the patterns within massive amounts of brain wave data, uncovering patterns that occur at extremely high frequencies that have never been described before and challenge foundational, long-held conceptions of the neurological basis of sleep and wake. ..."

From the abstract:

"The most robust and reliable signatures of brain states are enriched in rhythms between 0.1 and 20 Hz. Here we address the possibility that the fundamental unit of brain state could be at the scale of milliseconds and micrometers. By analyzing high-resolution neural activity recorded in ten mouse brain regions over 24 h, we reveal that brain states are reliably identifiable (embedded) in fast, nonoscillatory activity. Sleep and wake states could be classified from 100 to 101 ms of neuronal activity sampled from 100 µm of brain tissue. In contrast to canonical rhythms, this embedding persists above 1,000 Hz. This high-frequency embedding is robust to substates, sharp-wave ripples and cortical on/off states. Individual regions intermittently switched states independently of the rest of the brain, and such brief state discontinuities coincided with brief behavioral discontinuities. Our results suggest that the fundamental unit of state in the brain is consistent with the spatial and temporal scale of neuronal computation."

Our brains take naps while we're awake – and wake when we're asleep

Scientists find that small regions of the brain can take micro-naps while the rest of the brain is awake and vice versa (original news release) The study more generally shows how previously ignored fast brain waves define basic patterns of sleep and wake

A nonoscillatory, millisecond-scale embedding of brain state provides insight into behavior (no public access)