BI 245 Dan Levenstein: Neuro-AI, Dynamics, and Model Systems
Daniel Levenstein discusses spontaneous neural activity during sleep and its links to learning, memory and navigation. The conversation explores AI models as tools for understanding hippocampal and cortical dynamics, the relationship between experiments and theory, cognitive maps, world models, spiking networks and transformers. It also addresses the transition from postdoctoral researcher to running a laboratory. The episode was published on 2 September 2026 and runs for 1 hour, 36 minutes and 11 seconds.
Research Technician - Gonzalez Lab
The Gonzalez Lab at UCSF is recruiting a research technician for interdisciplinary work on vocal communication, social behavior, sleep, and neural dynamics. The role combines bird behavior, high-density electrophysiology, optical imaging, closed-loop stimulation, custom instrument development, and Python or MATLAB analysis, with later opportunities to support human EEG and natural-speech studies.
Neural circuits underlying sleep structure and functions
Sleep is an active state critical for processing emotional memories encoded during waking in both humans and animals. There is a remarkable overlap between the brain structures and circuits active during sleep, particularly rapid eye-movement (REM) sleep, and the those encoding emotions. Accordingly, disruptions in sleep quality or quantity, including REM sleep, are often associated with, and precede the onset of, nearly all affective psychiatric and mood disorders. In this context, a major biomedical challenge is to better understand the underlying mechanisms of the relationship between (REM) sleep and emotion encoding to improve treatments for mental health. This lecture will summarize our investigation of the cellular and circuit mechanisms underlying sleep architecture, sleep oscillations, and local brain dynamics across sleep-wake states using electrophysiological recordings combined with single-cell calcium imaging or optogenetics. The presentation will detail the discovery of a 'somato-dendritic decoupling'in prefrontal cortex pyramidal neurons underlying REM sleep-dependent stabilization of optimal emotional memory traces. This decoupling reflects a tonic inhibition at the somas of pyramidal cells, occurring simultaneously with a selective disinhibition of their dendritic arbors selectively during REM sleep. Recent findings on REM sleep-dependent subcortical inputs and neuromodulation of this decoupling will be discussed in the context of synaptic plasticity and the optimization of emotional responses in the maintenance of mental health.
How do we sleep?
There is no consensus on if sleep is for the brain, body or both. But the difference in how we feel following disrupted sleep or having a good night of continuous sleep is striking. Understanding how and why we sleep will likely give insights into many aspects of health. In this talk I will outline our recent work on how the prefrontal cortex can signal to the hypothalamus to regulate sleep preparatory behaviours and sleep itself, and how other brain regions, including the ventral tegmental area, respond to psychosocial stress to induce beneficial sleep. I will also outline our work on examining the function of the glymphatic system, and whether clearance of molecules from the brain is enhanced during sleep or wakefulness.
Location, time and type of epileptic activity influence how sleep modulates epilepsy
Sleep and epilepsy are tightly interconnected: On the one hand disturbed sleep is known to negatively affect epilepsy, whereas on the other hand epilepsy negatively impacts sleep. In this talk, we leverage on the unique opportunity provided by simultaneous stereo-EEG and sleep recordings to disentangle these relationships. We will discuss latest evidence on if anatomy (temporal vs. extratemporal), time (early vs. late sleep), and type of epileptic activity (ictal vs. interictal) influence how epileptic activity is modulated by sleep. After this talk, attendees will have a more nuanced understanding of the contributions of location, time and type of epileptic activity in the relationship between sleep and epilepsy.
Sleep, development and chromatin regulation in autism
Multimodal tracking of motor activity, sleep and mood
This talk will (1) describe patterns and correlates of objectively assessed motor activity (2) present findings on the inter-relationships among motor activity, sleep and circadian rhythms and mood disorders; (3) describe potential of cross species studies of motor activity and related systems to inform human chronobiology research
Light-induced moderations in vitality and sleep in the field
Retinal light exposure is modulated by our behavior, and light exposure patterns show strong variations within and between persons. Yet, most laboratory studies investigated influences of constant lighting settings on human daytime functioning and sleep. In this presentation, I will discuss a series of studies investigating light-induced moderations in sleepiness, vitality and sleep, with a strong focus on the temporal dynamics in these effects, and the bi-directional relation between persons' light profiles and their behavior.
The impact of spaceflight on sleep and circadian rhythms
What happens to human sleep and circadian rhythms in space? There are many challenges that affect sleep in space, including unusual patterns of light exposure and the influence of microgravity. This talk will review the causes and consequences of sleep loss and circadian misalignment during spaceflight and will discuss how missions to the Moon and Mars will be different than missions to the International Space Station.
How sleep contributes to visual perceptual learning
Sleep is crucial for the continuity and development of life. Sleep-related problems can alter brain function, and cause potentially severe psychological and behavioral consequences. However, the role of sleep in our mind and behavior is far from clear. In this talk, I will present our research on how sleep may play a role in visual perceptual learning (VPL) by using simultaneous magnetic resonance spectroscopy and polysomnography in human subjects. We measured the concentrations of neurotransmitters in the early visual areas during sleep and obtained the excitation/inhibition (E/I) ratio which represents the amount of plasticity in the visual system. We found that the E/I ratio significantly increased during NREM sleep while it decreased during REM sleep. The E/I ratio during NREM sleep was correlated with offline performance gains by sleep, while the E/I ratio during REM sleep was correlated with the amount of learning stabilization. These suggest that NREM sleep increases plasticity, while REM sleep decreases it to solidify once enhanced learning. NREM and REM sleep may play complementary roles, reflected by significantly different neurochemical processing, in VPL.
The Brain Conference (the Guarantors of Brain)
Join the Brain Conference on 24-25 February 2022 for the opportunity to hear from neurology’s leading scientists and clinicians. The two-day virtual programme features clinical teaching talks and research presentations from expert speakers including neuroscientist Professor Gina Poe, and the winner of the 2021 Brain Prize, neurologist Professor Peter Goadsby." "Tickets for The Brain Conference 2022 cost just £30, but register with promotional code BRAINCONEM20 for a discounted rate of £25.
CNStalk: Being awake while asleep, being asleep while awake
The Brain Conference (the Guarantors of Brain)
Join the Brain Conference on 24-25 February 2022 for the opportunity to hear from neurology’s leading scientists and clinicians. The two-day virtual programme features clinical teaching talks and research presentations from expert speakers including neuroscientist Professor Gina Poe, and the winner of the 2021 Brain Prize, neurologist Professor Peter Goadsby." "Tickets for The Brain Conference 2022 cost just £30, but register with promotional code BRAINCONEM20 for a discounted rate of £25.
Online "From Bench to Bedside" Neurosciences Symposium
2 Keynote lectures :“Homeostatic control of sleep in the fly"and “Management of Intracerebral Haemorrhage – where is the evidence?” and 2 sessions: "Cortical top-down information processing” and “Virtual/augmented reality and its implications for the clinic”
Mechanisms of sleep-seizure interactions in tuberous sclerosis and other mTORpathies
An intriguing, relatively unexplored therapeutic avenue to investigate epilepsy is the interaction of sleep mechanisms and seizures. Multiple lines of clinical observations suggest a strong, bi-directional relationship between epilepsy and sleep. Epilepsy and sleep disorders are common comorbidities. Seizures occur more commonly in sleep in many types of epilepsy, and in turn, seizures can cause disrupted sleep. Sudden unexplained death in epilepsy (SUDEP) is strongly associated with sleep. The biological mechanisms underlying this relationship between seizures and sleep are poorly understood, but if better delineated, could offer novel therapeutic approaches to treating both epilepsy and sleep disorders. In this presentation, I will explore this sleep-seizure relationship in mouse models of epilepsy. First, I will present general approaches for performing detailed longitudinal sleep and vigilance state analysis in mice, including pre-weanling neonatal mice. I will then discuss recent data from my laboratory demonstrating an abnormal sleep phenotype in a mouse model of the genetic epilepsy, tuberous sclerosis complex (TSC), and its relationship to seizures. The potential mechanistic basis of sleep abnormalities and sleep-seizure interactions in this TSC model will be investigated, focusing on the role of the mechanistic target of rapamycin (mTOR) pathway and hypothalamic orexin, with potential therapeutic applications of mTOR inhibitors and orexin antagonists. Finally, similar sleep-seizure interactions and mechanisms will be extended to models of acquired epilepsy due to status epilepticus-related brain injury.
Brain circuit dynamics in Action and Sleep
Our group focuses on brain computation, physiology and evolution, with a particular focus on network dynamics, sleep (evolution and mechanistic underpinnings), cortical computation (through the study of ancestral cortices), and sensorimotor processing. This talk will describe our recent results on the remarkable camouflage behavior of cuttlefish (action) and on brain activity in REM and NonREM in lizards (sleep). Both topics will focus on aspects of circuit dynamics.
Brain circuit dynamics in Action and Sleep
Our group focuses on brain computation, physiology and evolution, with a particular focus on network dynamics, sleep (evolution and mechanistic underpinnings), cortical computation (through the study of ancestral cortices), and sensorimotor processing. This talk will describe our recent results on the remarkable camouflage behavior of cuttlefish (action) and on brain activity in REM and NonREM in lizards (sleep). Both topics will focus on aspects of circuit dynamics.
Being awake while sleeping, being asleep while awake: consequences on cognition and consciousness
Sleep is classically presented as an all-or-nothing phenomenon. Yet, there is increasing evidence showing that sleep and wakefulness can actually intermingle and that wake-like and sleep-like activity can be observed concomitantly in different brain regions. I will here explore the implications of this conception of sleep as a local phenomenon for cognition and consciousness. In the first part of my presentation, I will show how local modulations of sleep depth during sleep could support the processing of sensory information by sleepers. I will also how, under certain circumstances, sleepers can learn while sleeping but also how they can forget. In the second part, I will show how the reverse phenomenon, sleep intrusions during waking, can explain modulations of attention. I will focus in particular on modulations of subjective experience and how the local sleep framework can inform our understanding of everyday phenomena such as mind wandering and mind blanking. Through this presentation and the exploration of both sleep and wakefulness, I will seek to connect changes in neurophysiology with changes in behaviour and subjective experience.
Second National Training Course on Sleep Medicine
Many patients presenting to neurology either have primary sleep disorders or suffer from sleep comorbidity. Knowledge on the diagnosis, differential diagnostic considerations, and management of these disorders is therefore mandatory for the general neurologist. This comprehensive course may serve to fulfill part of the preparation requirements for trainees seeking to complete the Royal College Examinations in Neurology. This training course is for R4 and R5 residents in Canadian neurology training programs as well as neurologists.
Evidence for the role of glymphatic dysfunction in the development of Alzheimer’s disease
Glymphatic perivascular exchange is supported by the astroglial water channel aquaporin-4 (AQP4), which localizes to perivascular astrocytic endfeet surrounding the cerebral vasculature. In aging mice, impairment of glymphatic function is associated with reduced perivascular AQP4 localization, yet whether these changes contribute to the development of neurodegenerative disease, such as Alzheimer’s disease (AD), remains unknown. Using post mortem human tissue, we evaluated perivascular AQP4 localization in the frontal cortical gray matter, white matter, and hippocampus of cognitively normal subjects and those with AD. Loss of perivascular and increasing cellular localization of AQP4 in the frontal gray matter was specifically associated with AD status, amyloid β (Aβ) and tau pathology, and cognitive decline in the early stages of disease. Using AAV-PHP.B to drive expression on non-perivascular AQP4 in wild type and Tg2576 (APPSwe, mouse model of Aβ deposition) mice, increased cellular AQP4 localization did not slow glymphatic function or change Aβ deposition. Using the Snta1 knockout line (which lacks perivascular AQP4 localization), we observed that loss AQP4 from perivascular endfeet slowed glymphatic function in wild type mice and accelerated Aβ plaque deposition in Tg2576 mice. These findings demonstrate that loss of perivascular AQP4 localization, and not increased cellular AQP4 localization, slows glymphatic function and promotes the development of AD pathology. To evaluate whether naturally occurring variation in the human AQP4 gene, or the alpha syntrophin (SNTA1), dystrobrevin (DTNA) or dystroglycan (DAG1) genes (whose products maintain perivascular AQP4 localization) confer risk for or protection from AD pathology or clinical progression, we evaluated 56 tag single nucleotide polymorphisms (SNPs) across these genes for association with CSF AD biomarkers, MRI measures of cortical and hippocampal atrophy, and longitudinal cognitive decline in the Alzheimer’s Disease Neuroimaging Initiative I (ADNI I) cohort. We identify 25 different significant associations between AQP4, SNTA1, DTNA, and DAG1 tag SNPs and phenotypic measures of AD pathology and progression. These findings provide complimentary human genetic evidence for the contribution of perivascular glymphatic dysfunction to the development of AD in human populations.
Active sleep in flies: the dawn of consciousness
The brain is a prediction machine. Yet the world is never entirely predictable, for any animal. Unexpected events are surprising and this typically evokes prediction error signatures in animal brains. In humans such mismatched expectations are often associated with an emotional response as well. Appropriate emotional responses are understood to be important for memory consolidation, suggesting that valence cues more generally constitute an ancient mechanism designed to potently refine and generalize internal models of the world and thereby minimize prediction errors. On the other hand, abolishing error detection and surprise entirely is probably also maladaptive, as this might undermine the very mechanism that brains use to become better prediction machines. This paradoxical view of brain functions as an ongoing tug-of-war between prediction and surprise suggests a compelling new way to study and understand the evolution of consciousness in animals. I will present approaches to studying attention and prediction in the tiny brain of the fruit fly, Drosophila melanogaster. I will discuss how an ‘active’ sleep stage (termed rapid eye movement – REM – sleep in mammals) may have evolved in the first animal brains as a mechanism for optimizing prediction in motile creatures confronted with constantly changing environments. A role for REM sleep in emotional regulation could thus be better understood as an ancient sleep function that evolved alongside selective attention to maintain an adaptive balance between prediction and surprise. This view of active sleep has some interesting implications for the evolution of subjective awareness and consciousness.
Investigating the neural mechanisms of spatial attention biases during sleep onset
Why we all need a good night’s sleep
We seek to determine how circadian rhythms and sleep are integrated with physiological processes to provide optimal fitness and health. Using initially a Drosophila model, and more recently also mammalian models, we have found that aspects of the blood brain barrier (BBB) are controlled by the circadian clock. BBB properties are also influenced by sleep:wake state in Drosophila, and, in fact, appear to be contribute to functions of sleep. This and other work, which implicates sleep in the regulation of metabolic processes, is providing insights into sleep function
Imaging memory consolidation in wakefulness and sleep
New memories are initially labile and have to be consolidated into stable long-term representations. Current theories assume that this is supported by a shift in the neural substrate that supports the memory, away from rapidly plastic hippocampal networks towards more stable representations in the neocortex. Rehearsal, i.e. repeated activation of the neural circuits that store a memory, is thought to crucially contribute to the formation of neocortical long-term memory representations. This may either be achieved by repeated study during wakefulness or by a covert reactivation of memory traces during offline periods, such as quiet rest or sleep. My research investigates memory consolidation in the human brain with multivariate decoding of neural processing and non-invasive in-vivo imaging of microstructural plasticity. Using pattern classification on recordings of electrical brain activity, I show that we spontaneously reprocess memories during offline periods in both sleep and wakefulness, and that this reactivation benefits memory retention. In related work, we demonstrate that active rehearsal of learning material during wakefulness can facilitate rapid systems consolidation, leading to an immediate formation of lasting memory engrams in the neocortex. These representations satisfy general mnemonic criteria and cannot only be imaged with fMRI while memories are actively processed but can also be observed with diffusion-weighted imaging when the traces lie dormant. Importantly, sleep seems to hold a crucial role in stabilizing the changes in the contribution of memory systems initiated by rehearsal during wakefulness, indicating that online and offline reactivation might jointly contribute to forming long-term memories. Characterizing the covert processes that decide whether, and in which ways, our brains store new information is crucial to our understanding of memory formation. Directly imaging consolidation thus opens great opportunities for memory research.
The suprachiasmatic nucleus: the brain's circadian clock
Sleep and all of the other circadian rhythms that adapt us to the 24 hour world are controlled by the suprachiasmatic nucleus (SCN), the brain's central circadian clock. And yet, the SCN consists of only 20,000 neurons and astrocytes, so what makes it such a powerful clock, able to set the tempo to our lives? Professor Hastings will consider the cell-autonomus and neural circuit-level mechanisms that sustain the SCN clock and how it regulates rest, activity and sleep.
Spatiotemporal patterns of neocortical activity around hippocampal sharp-wave ripples
Neocortical-hippocampal interactions during off-line periods such as slow-wave sleep are implicated in memory processing. In particular, recent memory traces are replayed in hippocampus during some sharp-wave ripple (SWR) events, and these replay events are positively correlated with neocortical memory trace reactivation. A prevalent model is that SWR arise ‘spontaneously’ in CA3 and propagate recent memory ‘indices’ outward to the neocortex to enable memory consolidation there; however, the spatiotemporal distribution of neocortical activation relative to SWR is incompletely understood. We used wide-field optical imaging to study voltage and glutamate release transients in dorsal neocortex in relation to CA1 multiunit activity (MUA) and SWR of sleeping and urethane anesthetized mice. Modulation of voltage and glutamate release signals in relation to SWRs varied across superficial neocortical regions, and it was largest in posteromedial regions surrounding retrosplenial cortex (RSC), which receives strong hippocampal output connections. Activity tended to spread sequentially from more medial towards more lateral regions. Contrary to the unidirectional hypothesis, activation exhibited a continuum of timing relative to SWRs, varying from neocortex leading to neocortex lagging the SWRs (± ~250 msec). The timing continuum was correlated with the skewness of peri-SWR hippocampal MUA and with a tendency for some SWR to occur in clusters. Thus, contrary to the model in which SWRs arise spontaneously in hippocampus, neocortical activation often precedes SWRs and may thus constitute a trigger event in which neocortical information seeds associative reactivation of hippocampal ‘indices’.
A metabolic function of the hippocampal sharp wave-ripple
The hippocampal formation has been implicated in both cognitive functions as well as the sensing and control of endocrine states. To identify a candidate activity pattern which may link such disparate functions, we simultaneously measured electrophysiological activity from the hippocampus and interstitial glucose concentrations in the body of freely behaving rats. We found that clusters of sharp wave-ripples (SPW-Rs) recorded from both dorsal and ventral hippocampus reliably predicted a decrease in peripheral glucose concentrations within ~10 minutes. This correlation was less dependent on circadian, ultradian, and meal-triggered fluctuations, it could be mimicked with optogenetically induced ripples, and was attenuated by pharmacogenetically suppressing activity of the lateral septum, the major conduit between the hippocampus and subcortical structures. Our findings demonstrate that a novel function of the SPW-R is to modulate peripheral glucose homeostasis and offer a mechanism for the link between sleep disruption and blood glucose dysregulation seen in type 2 diabetes and obesity.
Sleep and the gut
Sleep is generally associated with the brain but poor sleep impacts the entire body - many diseases are caused or exacerbated by sleep loss. Our work is uncovering ways in which sleep and the body interact. We found a special, two-way relationship between sleep and the gut: the gut is uniquely impacted by sleep loss, and it actively controls sleep quality. These findings could help us understand the origins of sleep as well as develop strategies to offset the negative consequences of inadequate sleep.
Markers of brain connectivity and sleep-dependent restoration: basic research and translation into clinical populations
The human brain is a heavily interconnected structure giving rise to complex functions. While brain functionality is mostly revealed during wakefulness, the sleeping brain might offer another view into physiological and pathological brain connectivity. Furthermore, there is a large body of evidence supporting that sleep mediates plastic changes in brain connectivity. Although brain plasticity depends on environmental input which is provided in the waking state, disconnection during sleep might be necessary for integrating new into existing information and at the same time restoring brain efficiency. In this talk, I will present structural, molecular, and electrophysiological markers of brain connectivity and sleep-dependent restoration that we have evaluated using Magnetic Resonance Imaging and electroencephalography in a healthy population. In a second step, I will show how we translated the gained findings into two clinical populations in which alterations in brain connectivity have been described, the neuropsychiatric disorder attention-deficit/hyperactivity disorder (ADHD) and the neurologic disorder thalamic ischemic stroke.
Local sleep regulation and its implications for cognition and brain plasticity
Sleep has been classically described as an all-or-nothing global phenomenon. However, a growing body of evidence indicates that typical sleep hallmarks, such as slow waves and spindles, occur and are regulated locally. I will present here evidence indicating that slow waves, in particular, may be related with, and offer a read-out of, local and long-range brain connectivity. In fact, slow waves do not only track changes related to both experience-dependent plasticity and brain maturation during development, but also appear to be actively involved in the fine regulation of brain plasticity and in the removal of metabolic wastes. I will also show that, consistent with a local regulation of sleep, slow waves can often occur locally during wakefulness, with an incidence that varies as a function of time spent awake and of previous rest. These waking slow waves are associated with impaired performance during cognitive tasks and may contribute to explain attention lapses and errors commonly associated with insufficient sleep.
Neurological consequences of COVID-19
The speakers will outline how neurologists in Bristol have been research-active during the COVID-19 pandemic including our contribution to national and international surveillance programmes as well as initiating research studies such as an evaluation of the impact of COVID anxiety on sleep and neurodegeneration and determining whether vascular changes in the eye predict COVID-19 severity.
Circadian/Multidien Molecular Oscillations and Rhythmicity of Epilepsy
The occurrence of seizures at specific times of the day has been consistently observed for centuries in individuals with epilepsy. Electrophysiological recordings provide evidence that seizures have a higher probability of occurring at a given time during the night and day cycle in individuals with epilepsy – the seizure rush hour. Which mechanisms underly such circadian rhythmicity of seizures? Why don’t they occur every day at the same time? Which mechanisms may underly their occurrence outside the rush hour? I shall present a hypothesis: MORE - Molecular Oscillations and Rhythmicity of Epilepsy, a conceptual framework to study and understand the mechanisms underlying the circadian rhythmicity of seizures and their probabilistic nature. The core of the hypothesis is the existence of circa 24h oscillations of gene and protein expression throughout the body in different cells and organs. The orchestrated molecular oscillations control the rhythmicity of numerous body events, such as feeding and sleep. The concept developed here is that molecular oscillations may favor seizure genesis at preferred times, generating the condition for a seizure rush hour. However, the condition is not sufficient, as other factors are necessary for a seizure to occur. Studying these molecular oscillations may help us understand seizure genesis mechanisms and find new therapeutic targets and predictive biomarkers. The MORE hypothesis can be generalized to comorbidities and the slower multidien (week/month period) rhythmicity of seizures.
How sleep remodels the brain
50 years ago it was found that sleep somehow made memories better and more permanent, but neither sleep nor memory researchers knew enough about sleep and memory to devise robust, effective tests. Today the fields of sleep and memory have grown and what is now understood is astounding. Still, great mysteries remain. What is the functional difference between the subtly different slow oscillation vs the slow wave of sleep and do they really have opposite memory consolidation effects? How do short spindles (e.g. <0.5 s as in schizophrenia) differ in function from longer ones and are longer spindles key to integrating new memories with old? Is the nesting of slow oscillations together with sleep spindles and hippocampal ripples necessary? What happens if all else is fine but the neurochemical environment is altered? Does sleep become maladaptive and “cement” memories into the hippocampal warehouse where they are assembled, together with all of their emotional baggage? Does maladaptive sleep underlie post-traumatic stress disorder and other stress-related disorders? How do we optimize sleep characteristics for top emotional and cognitive function? State of the art findings and current hypotheses will be presented.
Dragons, Sleep, and the Claustrum
The mammalian claustrum, by virtue of its dense interconnectivity with cortex and other brain structures, has been hypothesized to mediate functions ranging from decision making to consciousness. I will be presenting experimental evidence for the existence of a claustrum in reptiles, its role in generating brain dynamics characteristic of sleep, and discuss our neuroetholgical approach towards understanding fundamental aspects of sleep and claustrum function.
A paradoxical kind of sleep In Drosophila melanogaster
The dynamic nature of sleep in most animals suggests distinct stages which serve different functions. Genetic sleep induction methods in animal models provide a powerful way to disambiguate these stages and functions, although behavioural methods alone are insufficient to accurately identify what kind of sleep is being engaged. In Drosophila, activation of the dorsal fan-shaped body (dFB) promotes sleep, but it remains unclear what kind of sleep this is, how the rest of the fly brain is behaving, or if any specific sleep functions are being achieved. Here, we developed a method to record calcium activity from thousands of neurons across a volume of the fly brain during dFB-induced sleep, and we compared this to the effects of a sleep-promoting drug. We found that drug-induced spontaneous sleep decreased brain activity and connectivity, whereas dFB sleep was not different from wakefulness. Paradoxically, dFB-induced sleep was found to be even deeper than drug- induced sleep. When we probed the sleeping fly brain with salient visual stimuli, we found that the activity of visually-responsive neurons was blocked by dFB activation, confirming a disconnect from the external environment. Prolonged optogenetic dFB activation nevertheless achieved a significant sleep function, by correcting visual attention defects brought on by sleep deprivation. These results suggest that dFB activation promotes a distinct form of sleep in Drosophila, where brain activity and connectivity remain similar to wakefulness, but responsiveness to external sensory stimuli is profoundly suppressed.
Sleep, semantic memory, and creative problem solving
Creative thought relies on the reorganisation of existing knowledge. Sleep is known to be important for creative thinking, but there is a debate about which sleep stage is most relevant, and why. I will address this issue by proposing that Rapid Eye Movement sleep, or 'REM', and Non-REM sleep facilitate creativity in different ways. Memory replay mechanisms in Non-REM can abstract rules from corpuses of learned information, while replay in REM may promote novel associations. I propose that the iterative interleaving of REM and Non-REM across a night boosts the formation of complex knowledge frameworks, and allows these frameworks to be restructured - thus facilitating creative thought. My talk will discuss experiments exploring these hypotheses, and the mechanisms for these processes.