Sleep In Memory Consolidation Research Articles

Prefrontal cortical ripples mediate top-down suppression of hippocampal reactivation during sleep memory consolidation.

Consolidation of initially encoded hippocampal representations in the neocortex through reactivation is crucial for long-term memory formation and is facilitated by the coordination of hippocampal sharp-wave ripples (SWRs) with cortical slow and spindle oscillations during non-REM sleep. Recent evidence suggests that high-frequency cortical ripples can also coordinate with hippocampal SWRs in support of consolidation; however, the contribution of cortical ripples to reactivation remains unclear. We used high-density, continuous recordings in the hippocampus (area CA1) and prefrontal cortex (PFC) over the course of spatial learning and show that independent PFC ripples dissociated from SWRs are prevalent in NREM sleep and predominantly suppress hippocampal activity. PFC ripples paradoxically mediate top-down suppression of hippocampal reactivation rather than coordination, and this suppression is stronger for assemblies that are reactivated during coordinated CA1-PFC ripples for consolidation of recent experiences. Further, we show non-canonical, serial coordination of independent cortical ripples with slow and spindle oscillations, which are known signatures of memory consolidation. These results establish a role for prefrontal cortical ripples in top-down regulation of behaviorally relevant hippocampal representations during consolidation.

A visual paired associate learning (vPAL) paradigm to study memory consolidation during sleep.

Sleep improves the consolidation and long-term stability of newly formed memories and associations. Most research on human declarative memory and its consolidation during sleep uses word-pair associations requiring exhaustive learning. In the present study, we present the visual paired association learning (vPAL) paradigm, in which participants learn new associations between images of celebrities and animals. The vPAL is based on a one-shot exposure that resembles learning in natural conditions. We tested if vPAL can reveal a role for sleep in memory consolidation by assessing the specificity of memory recognition, and the cued recall performance, before and after sleep. We found that a daytime nap improved the stability of recognition memory and discrimination abilities compared to identical intervals of wakefulness. By contrast, cued recall of associations did not exhibit significant sleep-dependent effects. High-density electroencephalography during naps further revealed an association between sleep spindle density and stability of recognition memory. Thus, the vPAL paradigm opens new avenues for future research on sleep and memory consolidation across ages and heterogeneous populations in health and disease.

Exploring the role of sleep stages in memory consolidation and cognitive function

The biological process of sleep is crucial for maintaining both physical and mental health. There are two separate stages of sleep, which are rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep. They have distinct characteristics and functions that contribute to memory consolidation or cognitive function. The role of each sleep stage in memory consolidation and cognitive function is crucial for optimizing sleep and promoting cognitive performance. This paper reviews the different sleep stages and their contribution to memory consolidation and cognitive function. The findings suggest that NREM sleep aids in transferring information from short-term to long-term memory, also plays an important role in consolidating declarative and procedural memories, and REM sleep is involved in emotional regulation and the integration of emotional information with existing memories. These conclusions highlight the significant role of sleep in memory consolidation and cognitive function.

0043 Modulation of ultra-slow calcium oscillation in the dentate gyrus during Non-REM sleep

Abstract Introduction The function of sleep in memory consolidation has been well established. Hippocampal CA1 and CA3 subregions are thought to be particularly important in this process. The current working hypothesis postulates that episodic memory traces captured during waking hours are replayed in the hippocampal CA1-CA3 areas and transferred to the cortex for long-term storage during sleep. Even though the sensory and spatial information from higher-order cortical areas such as the entorhinal cortex primarily enters the hippocampus via the dentate gyrus (DG), this structure has always been considered as the “silent partner” in memory consolidation. Whether and how the captured memory traces are transferred from the DG toward the downstream hippocampal areas is less known. Methods Here, we used fiber photometry, two-photon calcium imaging, and EEG recording to examine the activity of DG during sleep. Results Strikingly, we found that DG cells are even more active during sleep than wakefulness and the calcium activity in the DG slowly oscillates during non-REM (NREM) sleep epochs. Furthermore, we also found that the cycles of this activity coinciding with microarousals are tightly locked to brief serotonin (5-HT) release during NREM sleep. Pharmacological blockade of 5-HT1a receptors abolished the calcium oscillations in the DG. Furthermore, genetic knockdown of 5-HT1a receptors in the DG leads to memory impairment in spatial and contextual memory tasks. Conclusion Together, our results indicate that ultra-slow calcium oscillations in the DG during NREM sleep are driven by serotonin fluctuations and they are required for memory consolidation. Support (if any)

Elucidation of the mechanisms underway in the brain during sleep with a focus on the circuit mechanisms that promote memory formation

Scientists have been unable to fully elucidate the mechanisms at work in the human brain during sleep. A particularly mysterious area is memory formation during sleep. Professor Masaki Takeda, Research Center for Brain Communication, the Kochi University of Technology, Japan, leads a team of researchers exploring brain behaviour and dynamism. A key focus is on human participants and what happens in their brains while sleeping, while a further element is looking at whether non-human primates have similar memory mechanisms to humans. A main goal for Takeda and the team is uncovering the causal role of neural activities during sleep in memory consolidation. As such, the researchers are attempting to noninvasively manipulate neural activity when human participants are sleeping and investigate how these manipulations affect memory performance after sleep. Using a combination of deep-learning decoding techniques and high spatiotemporal resolution of neural imaging by concurrent functional magnetic resonance imaging (fMRI) and electroencephalography (EEG), the team has developed a novel technique for detecting the replay activity that emerges as unstructured patterns of activations, overcoming challenges associated with the difference between spatial and semantic memory. In a recent project, Takeda and the team have been exploring brain circuit mechanisms during sleep that promote memory formation. The researchers are exploring whether the slow-oscillation neural activity during deep sleep (SO) in the frontal cortex during deep sleep has a causal role in memory consolidation in humans. This involves the manipulation of the phase of SOs using transcranial alternating current stimulation (tACS) whose phase is matched to that of SOs.

Is word learning capacity restored after a daytime nap?

Sleep is thought to be involved in the consolidation of new memories encoded during the day, as proposed by complementary learning systems accounts of memory. Other theories suggest that sleep's role in memory is not restricted to consolidation. The synaptic homeostasis hypothesis proposes that new learning is implemented in the brain through strengthening synaptic connections, a biologically costly process that gradually saturates encoding capacity during wake. During slow-wave sleep, synaptic strength is renormalized, thus restoring memory encoding ability. While the role of sleep in memory consolidation has been extensively documented, few human studies have explored the impact of sleep in restoring encoding ability, and none have looked at learning beyond episodic memory. In this registered report we test the predictions made by the complementary learning systems accounts and the synaptic homeostasis hypothesis regarding adult participants' ability to learn new words, and to integrate these words with existing knowledge. Participants took a polysomnographically-monitored daytime nap or remained awake prior to learning a set of new spoken words. Shortly after learning, and again on the following day, we measured participants' episodic memory for new words. We also assessed the degree to which newly learned words engage in competition with existing words. We predicted that sleep before encoding would result in better episodic memory for the words, and facilitate the overnight integration of new words with existing words. Based on existing literature and theory we further predicted that this restorative function is associated with slow-wave and sleep spindle activity. Our pre-registered analyses did not find a significant benefit of napping prior to encoding on word learning or integration. Exploratory analyses using a more sensitive measure of recall accuracy demonstrated significantly better performance in the nap condition compared to the no-nap condition in the immediate test. At the delayed test there was no longer a significant benefit of the nap. Of note, we found no significant effect of slow-wave activity prior to encoding on episodic memory or integration of newly learned words into the mental lexicon. However, we found that greater levels of Stage 2 sleep spindles were significantly associated with greater improvements in lexical competition from the immediate to the delayed test. Therefore, our results demonstrate some support for theories that implicate sleep spindles in restoring encoding capacity.

Sleep does not influence schema-facilitated motor memory consolidation.

Novel information is rapidly learned when it is compatible with previous knowledge. This "schema" effect, initially described for declarative memories, was recently extended to the motor memory domain. Importantly, this beneficial effect was only observed 24 hours-but not immediately-following motor schema acquisition. Given the established role of sleep in memory consolidation, we hypothesized that sleep following the initial learning of a schema is necessary for the subsequent rapid integration of novel motor information. Two experiments were conducted to investigate the effect of diurnal and nocturnal sleep on schema-mediated motor sequence memory consolidation. In Experiment 1, participants first learned an 8-element motor sequence through repeated practice (Session 1). They were then afforded a 90-minute nap opportunity (N = 25) or remained awake (N = 25) before learning a second motor sequence (Session 2) which was highly compatible with that learned prior to the sleep/wake interval. Experiment 2 was similar; however, Sessions 1 and 2 were separated by a 12-hour interval that included nocturnal sleep (N = 28) or only wakefulness (N = 29). For both experiments, we found no group differences in motor sequence performance (reaction time and accuracy) following the sleep/wake interval. Furthermore, in Experiment 1, we found no correlation between sleep features (non-REM sleep duration, spindle and slow wave activity) and post-sleep behavioral performance. The results of this research suggest that integration of novel motor information into a cognitive-motor schema does not specifically benefit from post-learning sleep.

Sleep Spindle Characteristics and Relationship with Memory Ability in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome.

Obstructive sleep apnea syndrome (OSAS) causes intermittent hypoxia and sleep disruption in the brain, resulting in cognitive dysfunction, but its pathogenesis is unclear. The sleep spindle wave is a transient neural event involved in sleep memory consolidation and synaptic plasticity. This study aimed to investigate the characteristics of sleep spindle activity and its relationship with memory ability in patients with OSAS. A total of 119 patients, who were divided into the OSAS group (n = 59, AHI ≥ 15) and control group (n = 60, AHI < 15) according to the Apnea Hypopnea Index (AHI), were enrolled and underwent polysomnography. Power spectral density (PSD) and omega complexity were used to analyze the characteristics of single and different brain regions of sleep spindles. Memory-related cognitive functions were assessed in all subjects, including logical memory, digit ordering, pattern recognition, spatial recognition and spatial working memory. The spindle PSD of the OSAS group was significantly slower than the control group, regardless of the slow, fast, or total spindle. The complexity of the spindles in the prefrontal and central region decreased significantly, whereas it increased in the occipital region. Sleep spindle PSD was positively correlated with logical memory and working memory. Spindle complexity was positively correlated with immediate logical and visual memory in the prefrontal region and positively correlated with immediate/delayed logical and working memory in the central region. In contrast, spindle complexity in the occipital region negatively correlated with delayed logical memory. Spindle hyperconnectivity in the prefrontal and central regions underlies declines in logical, visual and working memory and weak connections in the occipital spindles underlie the decline in delayed logical memory.

0228 Using Blue Light Therapy to Facilitate Recovery of Sleep and Psychological Functioning in PTSD

Abstract Introduction Sleep problems are often described as the “hallmark symptoms” of post-traumatic stress disorder (PTSD). Patients with PTSD show numerous disruptions of emotional functioning. Experimental evidence has shown that the ability to retain extinction memories following fear conditioning is impaired in people with PTSD. Because of the key role of sleep in memory consolidation and emotional regulation, we hypothesized that regulating sleep and circadian rhythms with morning blue-wavelength light therapy would facilitate emotional recovery and the ability to retain extinction memories. Methods Eighty-four individuals with PTSD (56 female; Age=31.38, SD=8.9) underwent a well-validated fear conditioning and extinction protocol and were then randomly assigned to receive either 6-weeks of BLUE (469 nm; n=44) or placebo AMBER (578 nm; n=40) morning light therapy for 30-minutes daily. Participants returned to undergo post-treatment extinction recall when exposed to the same previously conditioned stimuli, and a functional magnetic resonance imaging (fMRI) while the same images were presented. Participants also completed a variety of emotional and mental health outcome measures and wore an actigraph to measure sleep over the 6-weeks. Results There was a significant interaction between light condition and time in bed and total sleep time (p<.05) indicating significant increases in sleep with blue versus amber light over treatment. Additionally, declines in symptoms of PTSD on the Clinician Administered PTSD Scale (CAPS-5) correlated with improvements in sleep for the blue, but not the amber light, group (all p-values <.05). During the fear conditioning and extinction paradigm, blue light was associated with significantly greater extinction recall compared to the amber light condition (p=.05). Finally, blue light resulted in decreased fMRI activation within the right amygdala and increased activation within the ventromedial prefrontal cortex to the previously feared and extinguished stimuli. Conclusion Blue light treatment was more effective than amber placebo at increasing sleep quantity, shifting circadian bedtime, reducing PTSD symptom severity, facilitating the retention of extinction memories, and reducing neural fear responses to previously feared stimuli. We suggest that improvements in sleep led to greater consolidation of extinction memories. These findings suggest that blue light treatment may facilitate treatment gains by improving sleep. Support (If Any)

The role of sleep for episodic memory consolidation: Stabilizing or rescuing?

Prior studies suggest a role for sleep in memory consolidation, with specific contributions from slow oscillations and sleep spindles (Rasch & Born, 2013). However, recent studies failed to replicate sleep’s superiority over wake in strengthening memory against interference (Cordi & Rasch, 2021). The goal of the current study is to investigate whether sleep protects newly formed memory from unspecific interference induced by daytime experiences over 24 h, as well as to elucidate the sleep features that are involved. 56 healthy adults were randomly assigned to either the Sleep First or Wake First group. The Sleep First group encoded word pairs at night before sleep, while the Wake First group encoded word pairs in the morning before a day of wakefulness. Memory was tested 30 min, 12 h, and 24 h after encoding for both groups. The Sleep First group performed significantly better 12 h after encoding, replicating prior findings that memory is better after a period of sleep compared to wake. However, after 24 h, the two groups performed similarly. The Wake First group showed a positive correlation between overnight memory improvement and the theta and delta band power during slow wave sleep, an effect not found in the Sleep First group. These correlations suggest the possibility that after a day of waking interference, the brain recruits extra sleep resources to rescue memories from further forgetting. Our results are not consistent with prior studies showing a significant role for sleep in stabilizing memory from future interference, but they may suggest that sleep rescues memories after interference has occurred.

Handling, task complexity, time-of-day, and sleep deprivation as dynamic modulators of recognition memory in mice

Sleep is essential for optimal cognitive functioning. Although we lack a complete understanding of the role of sleep in memory consolidation, we know that various factors that disturb sleep or sleep quality have consequences for cognitive performance. Such factors can be unintended components of behavioral experiments on rodents and other experimental animals that generate differing results from different labs. These experimental variables include habituation to handling, intended or unintended sleep deprivation, task complexity, time of testing, and environmental features. We have examined how these variables impact recognition memory in C57BL/6 mice. Handled mice outperformed their non-handled counterparts across different combinations of delay phase duration and lighting conditions. Results also suggest that simple task recall is more resistant to diurnal variation and the impairing effects of sleep deprivation than is complex task recall. This study underscores the role of protocol and environmental factors in recognition memory and in conflicting results from different laboratories.

The use of rodent models to better characterize the relationship among epilepsy, sleep, and memory.

Epilepsy, a neurological disorder characterized by recurrent seizures, is known to be associated with impaired sleep and memory. Although the specific mechanisms underlying these impairments are uncertain, the known role of sleep in memory consolidation suggests a potential relationship may exist between seizure activity, disrupted sleep, and memory impairment. A possible mediator in this relationship is the sleep spindle, the characteristic electroencephalographic (EEG) feature of non-rapid-eye-movement (NREM) sleep in humans and other mammals. Growing evidence supports the idea that sleep spindles, having thalamic origin, may mediate the process of long-term memory storage and plasticity by generating neuronal conditions that favor these processes. To study this potential relationship, a single model in which memory, sleep, and epilepsy can be simultaneously observed is of necessity. Rodent models of epilepsy appear to fulfill this requirement. Not only do rodents express both sleep spindles and seizure-induced sleep disruptions, but they also allow researchers to invasively study neurobiological processes both pre- and post- epileptic onset via the artificial induction of epilepsy (a practice that cannot be carried out in human subjects). However, the degree to which sleep architecture differs between rodents and humans makes direct comparisons between the two challenging. This review addresses these challenges and concludes that rodent sleep studies are useful in observing the functional roles of sleep and how they are affected by epilepsy.

Sleep and Memory Consolidation Dysfunction in Psychiatric Disorders: Evidence for the Involvement of Extracellular Matrix Molecules.

Sleep disturbances and memory dysfunction are key characteristics across psychiatric disorders. Recent advances have revealed insight into the role of sleep in memory consolidation, pointing to key overlap between memory consolidation processes and structural and molecular abnormalities in psychiatric disorders. Ongoing research regarding the molecular mechanisms involved in memory consolidation has the potential to identify therapeutic targets for memory dysfunction in psychiatric disorders and aging. Recent evidence from our group and others points to extracellular matrix molecules, including chondroitin sulfate proteoglycans and their endogenous proteases, as molecules that may underlie synaptic dysfunction in psychiatric disorders and memory consolidation during sleep. These molecules may provide a therapeutic targets for decreasing strength of reward memories in addiction and traumatic memories in PTSD, as well as restoring deficits in memory consolidation in schizophrenia and aging. We review the evidence for sleep and memory consolidation dysfunction in psychiatric disorders and aging in the context of current evidence pointing to the involvement of extracellular matrix molecules in these processes.

Availability of food determines the need for sleep in memory consolidation.

Summary:Sleep remains a major mystery of biology, with little understood about its basic function. One of the most commonly proposed functions for sleep is the consolidation of memory1–3. However, as conditions like starvation require the organism to be awake and active4, the ability to switch to a memory consolidation mechanism that is not contingent on sleep may confer an evolutionary advantage. Here, we identify a novel adaptive circuit-based mechanism that enables Drosophila to form sleep-dependent and sleep-independent memory. Flies fed after appetitive conditioning needed increased sleep for memory consolidation, but flies starved after training did not require sleep to form memories. Memory in fed flies is mediated by the anterior-posterior α’/β’ neurons of the mushroom body (MB), while memory under starvation is mediated by medial α’/β’ neurons. Sleep-dependent and sleep-independent memory rely upon distinct dopaminergic neurons and corresponding MB output neurons. However, sleep and memory are coupled such that mushroom body neurons required for sleep-dependent memory also promote sleep. Flies lacking Neuropeptide F display sleep-dependent memory even when starved, suggesting that circuit selection is determined by hunger. This plasticity in memory circuits enables flies to retain essential information in changing environments.

Slow Wave Sleep Is a Promising Intervention Target for Alzheimer's Disease.

Alzheimer’s disease (AD) is the major cause of dementia, characterized by the presence of amyloid-beta plaques and neurofibrillary tau tangles. Plaques and tangles are associated with sleep-wake cycle disruptions, including the disruptions in non-rapid eye movement (NREM) slow wave sleep (SWS). Alzheimer’s patients spend less time in NREM sleep and exhibit decreased slow wave activity (SWA). Consistent with the critical role of SWS in memory consolidation, reduced SWA is associated with impaired memory consolidation in AD patients. The aberrant SWA can be modeled in transgenic mouse models of amyloidosis and tauopathy. Animal models exhibited slow wave impairments early in the disease progression, prior to the deposition of amyloid-beta plaques, however, in the presence of abundant oligomeric amyloid-beta. Optogenetic rescue of SWA successfully halted the amyloid accumulation and restored intraneuronal calcium levels in mice. On the other hand, optogenetic acceleration of slow wave frequency exacerbated amyloid deposition and disrupted neuronal calcium homeostasis. In this review, we summarize the evidence and the mechanisms underlying the existence of a positive feedback loop between amyloid/tau pathology and SWA disruptions that lead to further accumulations of amyloid and tau in AD. Moreover, since SWA disruptions occur prior to the plaque deposition, SWA disruptions may provide an early biomarker for AD. Finally, we propose that therapeutic targeting of SWA in AD might lead to an effective treatment for Alzheimer’s patients.

REM sleep deprivation impairs retrieval, but not reconsolidation, of methamphetamine reward memory in male rats

Susceptibility to interference can be a result of memory retrieval and reconsolidation. Given the fact that addiction develops through the neural mechanisms of learning and memory, it would not be surprising that a consolidated drug reward memory may also be susceptible to interference following retrieval/reconsolidation. Due to the critical role of sleep in memory consolidation, sleep deprivation (SD) has been shown to impair memory. Therefore, the major objective of this study was to investigate the effect of rapid eye movement (REM) sleep deprivation (RSD) on the retrieval and reconsolidation of methamphetamine (METH) reward memory in male rats. The animals were trained to acquire METH-induced CPP (2 mg/kg, i.p.). METH reward memory was then reactivated/retrieved in the drug-paired chamber during a drug-free (memory reactivation) session. A period of 48-h RSD paradigm using the multiple platform technique resulted in persistent deficits in the retrieval of METH reward memory. Nevertheless, the same protocol of RSD, which was conducted immediately after the memory reactivation, did not affect the reconsolidation of METH reward memory. Additionally, the RSD episode induced a temporary potentiation of METH-induced hyperlocomotion. Our findings would seem to suggest that sleep is involved in the retrieval, but not reconsolidation, of METH reward memory. The results may also demonstrate that RSD mimics the effects of METH on locomotor activity. The results of this study, therefore, support the idea that sleep is involved in the processing of METH reward memory which can be considered for further investigations to manage the relapse associated with drug-related memory.

Sleep and memory consolidation

Memory consolidation refers to processes following the encoding of new information and allowing the transformation of labile and interference-sensitive memory traces into stable representations. The role of sleep in these processes was highlighted more than one century ago, and if the modalities of this crucial function (passive, permissive or active role), the type of memory concerned, and the respective role of different sleep stages have been highly debated, the complementary involvement of different vigilance stages-associated specific cerebral activity in memory stabilization and re-organization is now widely accepted. Several arguments have been provided toward an active role of sleep in memory consolidation: – deleterious effect of post-learning sleep deprivation (or of several sleep disorders) on delayed recall performance; – post-learning sleep structural changes, depending on the learning task type and correlated with delayed recall performance; – improvement in memory performance induced by neuromodulation or targeted reactivation techniques applied during sleep. The hippocampus plays a key role in these processes via sharp wave-ripples, high frequency oscillations associated with reactivation of neuronal activity sequences, synchronized with Non-Rapid Eye Movement sleep (N-REM) oscillations such as spindles and slow waves. This temporally fine-tuned coupling allow transfer of information from hippocampus to neocortex. Recent works argue for a sequential involvement of NREM and REM sleep: irrelevant information are tagged to be erased (synaptic downscaling), while other synapses are reactivated and potentiated, allowing then new memories to be incorporated into old representations and providing condition for their long-term stabilization.

Making Memories: Why Time Matters.

In the last decade advances in human neuroscience have identified the critical importance of time in creating long-term memories. Circadian neuroscience has established biological time functions via cellular clocks regulated by photosensitive retinal ganglion cells and the suprachiasmatic nuclei. Individuals have different circadian clocks depending on their chronotypes that vary with genetic, age, and sex. In contrast, social time is determined by time zones, daylight savings time, and education and employment hours. Social time and circadian time differences can lead to circadian desynchronization, sleep deprivation, health problems, and poor cognitive performance. Synchronizing social time to circadian biology leads to better health and learning, as demonstrated in adolescent education. In-day making memories of complex bodies of structured information in education is organized in social time and uses many different learning techniques. Research in the neuroscience of long-term memory (LTM) has demonstrated in-day time spaced learning patterns of three repetitions of information separated by two rest periods are effective in making memories in mammals and humans. This time pattern is based on the intracellular processes required in synaptic plasticity. Circadian desynchronization, sleep deprivation, and memory consolidation in sleep are less well-understood, though there has been considerable progress in neuroscience research in the last decade. The interplay of circadian, in-day and sleep neuroscience research are creating an understanding of making memories in the first 24-h that has already led to interventions that can improve health and learning.

Computational models of memory consolidation and long-term synaptic plasticity during sleep.

The brain stores memories by persistently changing the connectivity between neurons. Sleep is known to be critical for these changes to endure. Research on the neurobiology of sleep and the mechanisms of long-term synaptic plasticity has provided data in support of various theories of how brain activity during sleep affects long-term synaptic plasticity. The experimental findings - and therefore the theories - are apparently quite contradictory, with some evidence pointing to a role of sleep in the forgetting of irrelevant memories, whereas other results indicate that sleep supports the reinforcement of the most valuable recollections. A unified theoretical framework is in need. Computational modeling and simulation provide grounds for the quantitative testing and comparison of theoretical predictions and observed data, and might serve as a strategy to organize the rather complicated and diverse pool of data and methodologies used in sleep research. This review article outlines the emerging progress in the computational modeling and simulation of the main theories on the role of sleep in memory consolidation.

Dreaming of a learning task is associated with enhanced memory consolidation: Replication in an overnight sleep study.

Sleep following learning benefits memory. One model attributes this effect to the iterative "reactivation" of memory traces in the sleeping brain, demonstrated in animal models. Although technical limitations prohibit using the same methods to observe memory reactivation in the human brain, the study of mental activity during sleep provides an alternative method of observing memory activation during sleep. In fact, the content of dream experience may reflect the process of memory reactivation and consolidation in the sleeping brain. In line with this hypothesis, we previously reported that dreaming about a spatial learning task during a nap strongly predicts subsequent performance improvements. Here, we replicate this observation in an overnight sleep study, for the first time demonstrating that pre-sleep training on a virtual maze navigation task is reflected in dreams reported from all phases of sleep, with unambiguous representation of the task in dream content associated with improved next-morning performance. These observations are consistent with reactivation-based models of memory consolidation in sleep, confirming our earlier finding that the cognitive-level activation of recent experience during sleep is associated with subsequent performance gains.