A noradrenergic-hypothalamic neural substrate for stress-induced sleep disturbances.

In our daily life, we are exposed to uncontrollable and stressful events that disrupt our sleep. However, the underlying neural mechanisms deteriorating the quality of non-rapid eye movement sleep (NREMs) and REM sleep are largely unknown. Here, we show in mice that acute psychosocial stress disrupts sleep by increasing brief arousals (microarousals [MAs]), reducing sleep spindles, and impairing infraslow oscillations in the spindle band of the electroencephalogram during NREMs, while reducing REMs. This poor sleep quality was reflected in an increased number of calcium transients in the activity of noradrenergic (NE) neurons in the locus coeruleus (LC) during NREMs. Opto- and chemogenetic LC-NE activation in naïve mice is sufficient to change the sleep microarchitecture similar to stress. Conversely, chemogenetically inhibiting LC-NE neurons reduced MAs during NREMs and normalized their number after stress. Specifically inhibiting LC-NE neurons projecting to the preoptic area of the hypothalamus (POA) decreased MAs and enhanced spindles and REMs after stress. Optrode recordings revealed that stimulating LC-NE fibers in the POA indeed suppressed the spiking activity of POA neurons that are activated during sleep spindles and REMs and inactivated during MAs. Our findings reveal that changes in the dynamics of the stress-regulatory LC-NE neurons during sleep negatively affect sleep quality, partially through their interaction with the POA.

The Hierarchy of Coupled Sleep Oscillations Reverses with Aging in Humans.

A well orchestrated coupling hierarchy of slow waves and spindles during slow-wave sleep supports memory consolidation. In old age, the duration of slow-wave sleep and the number of coupling events decrease. The coupling hierarchy deteriorates, predicting memory loss and brain atrophy. Here, we investigate the dynamics of this physiological change in slow wave-spindle coupling in a frontocentral electroencephalography position in a large sample (N = 340; 237 females, 103 males) spanning most of the human life span (age range, 15-83 years). We find that, instead of changing abruptly, spindles gradually shift from being driven by slow waves to driving slow waves with age, reversing the coupling hierarchy typically seen in younger brains. Reversal was stronger the lower the slow-wave frequency, and starts around midlife (age range, ∼40-48 years), with an established reversed hierarchy between 56 and 83 years of age. Notably, coupling strength remains unaffected by age. In older adults, deteriorating slow wave-spindle coupling, measured using the phase slope index (PSI) and the number of coupling events, is associated with blood plasma glial fibrillary acidic protein levels, a marker for astrocyte activation. Data-driven models suggest that decreased sleep time and higher age lead to fewer coupling events, paralleled by increased astrocyte activation. Counterintuitively, astrocyte activation is associated with a backshift of the coupling hierarchy (PSI) toward a "younger" status along with increased coupling occurrence and strength, potentially suggesting compensatory processes. As the changes in coupling hierarchy occur gradually starting at midlife, we suggest there exists a sizable window of opportunity for early interventions to counteract undesirable trajectories associated with neurodegeneration.SIGNIFICANCE STATEMENT Evidence accumulates that sleep disturbances and cognitive decline are bidirectionally and causally linked, forming a vicious cycle. Improving sleep quality could break this cycle. One marker for sleep quality is a clear hierarchical structure of sleep oscillations. Previous studies showed that sleep oscillations decouple in old age. Here, we show that, rather, the hierarchical structure gradually shifts across the human life span and reverses in old age, while coupling strength remains unchanged. This shift is associated with markers for astrocyte activation in old age. The shifting hierarchy resembles brain maturation, plateau, and wear processes. This study furthers our comprehension of this important neurophysiological process and its dynamic evolution across the human life span.

Blindness affects the developmental trajectory of the sleeping brain.

Sleep plays a crucial role in brain development, sensory information processing, and consolidation. Sleep spindles are markers of these mechanisms as they mirror the activity of the thalamocortical circuits. Spindles can be subdivided into two groups, slow (10-13 Hz) and fast (13-16 Hz), which are each associated with different functions. Specifically, fast spindles oscillate in the high-sigma band and are associated with sensorimotor processing, which is affected by visual deprivation. However, how blindness influences spindle development has not yet been investigated. We recorded nap video-EEG of 50 blind/severely visually impaired (BSI) and 64 sighted children aged 5 months to 6 years old. We considered aspects of both macro- and micro-structural spindles. The BSI children lacked the evolution of developmental spindles within the central area. Specifically, young BSI children presented low central high-sigma and high-beta (25-30 Hz) event-related spectral perturbation and showed no signs of maturational decrease. High-sigma and high-beta activity in the BSI group correlated with clinical indices predicting perceptual and motor disorders. Our findings suggest that fast spindles are pivotal biomarkers for identifying an early developmental deviation in BSI children. These findings are critical for initial therapeutic intervention.

The neurophysiology of closed-loop auditory stimulation in sleep: A magnetoencephalography study.

Closed-loop auditory stimulation (CLAS) is a brain modulation technique in which sounds are timed to enhance or disrupt endogenous neurophysiological events. CLAS of slow oscillation up-states in sleep is becoming a popular tool to study and enhance sleep's functions, as it increases slow oscillations, evokes sleep spindles and enhances memory consolidation of certain tasks. However, few studies have examined the specific neurophysiological mechanisms involved in CLAS, in part because of practical limitations to available tools. To evaluate evidence for possible models of how sound stimulation during brain up-states alters brain activity, we simultaneously recorded electro- and magnetoencephalography in human participants who received auditory stimulation across sleep stages. We conducted a series of analyses that test different models of pathways through which CLAS of slow oscillations may affect widespread neural activity that have been suggested in literature, using spatial information, timing and phase relationships in the source-localized magnetoencephalography data. The results suggest that auditory information reaches ventral frontal lobe areas via non-lemniscal pathways. From there, a slow oscillation is created and propagated. We demonstrate that while the state of excitability of tissue in auditory cortex and frontal ventral regions shows some synchrony with the electroencephalography (EEG)-recorded up-states that are commonly used for CLAS, it is the state of ventral frontal regions that is most critical for slow oscillation generation. Our findings advance models of how CLAS leads to enhancement of slow oscillations, sleep spindles and associated cognitive benefits and offer insight into how the effectiveness of brain stimulation techniques can be improved.

Structural Brain Correlates of Sleep Microstructure in Spinocerebellar Ataxia Type 2 and its Role on Clinical Phenotype.

The influence of brain atrophy on sleep microstructure in Spinocerebellar Ataxias (SCAs) has not been extensively explored limiting the use of these sleep traits as surrogate biomarkers of neurodegeneration and clinical phenotype. The objective of the study is to explore the relationship between sleep microstructure and brain atrophy in SCA2 and its role in the clinical phenotype. Fourteen SCA2 mutation carriers (7 pre-manifest and 7 manifest subjects) underwent polysomnographic, structural MRI, and clinical assessments. Particularly, markers of REM and non-REM sleep microstructure, measures of cerebellar and brainstem atrophy, and clinical scores were analyzed through correlation and mediation analyses. The sleep spindle activity exhibited a negative correlation with the number of trials required to complete the verbal memory test (VMT), and a positive correlation with the cerebellar volume, but the significance of the latter correlation did not survive multiple testing corrections. However, the causal mediation analyses unveiled that sleep spindle activity significantly mediates the association between cerebellar atrophy and VMT performance. Regarding REM sleep, both phasic EMG activity and REM sleep without atonia exhibited significant associations with pontine atrophy and disease severity measures. However, they did not demonstrate a causal mediation effect between the atrophy measures and disease severity. Our study provides evidence about the association of the pontocerebellar atrophy with sleep microstructure in SCA2 offering insights into the cerebellar involvement in cognition via the control of the sleep spindle activity. Therefore, our findings may help to understand the disease pathogenesis and to better characterize sleep microstructure parameters as disease biomarkers.Clinical trial registration number (TRN): No applicable.

An acute bout of high-intensity exercise affects nocturnal sleep and sleep-dependent memory consolidation.

Acute exercise has been shown to affect long-term memory and sleep. However, it is unclear whether exercise-induced changes in sleep architecture are associated with enhanced memory. Recently, it has been shown that exercise followed by a nap improved declarative memory. Whether these effects transfer to night sleep and other memory domains has not yet been studied. Here, we investigate the influence of exercise on nocturnal sleep architecture and associations with sleep-dependent procedural and declarative memory consolidation. Nineteen subjects (23.68 ± 3.97 years) were tested in a balanced cross-over design. In two evening sessions, participants either exercised (high-intensity interval training) or rested immediately after encoding two memory tasks: (1) a finger tapping task and (2) a paired-associate learning task. Subsequent nocturnal sleep was recorded by polysomnography. Retrieval was conducted the following morning. High-intensity interval training lead to an increased declarative memory retention (p = 0.047, d = 0.40) along with a decrease in REM sleep (p = 0.012, d = 0.75). Neither procedural memory nor NREM sleep were significantly affected. Exercise-induced changes in N2 showed a positive correlation with procedural memory retention which did not withstand multiple comparison correction. Exploratory analyses on sleep spindles and slow wave activity did not reveal significant effects. The present findings suggest an exercise-induced enhancement of declarative memory which aligns with changes in nocturnal sleep architecture. This gives additional support for the idea of a potential link between exercise-induced sleep modifications and memory formation which requires further investigation in larger scaled studies.

Sleep Spindle Generation Before and After Epilepsy Surgery: A Source Imaging Study in Children with Drug-Resistant Epilepsy.

INTRODUCTION: Literature lacks studies investigating the cortical generation of sleep spindles in drug-resistant epilepsy (DRE) and how they evolve after resection of the epileptogenic zone (EZ). Here, we examined sleep EEGs of children with focal DRE who became seizure-free after focal epilepsy surgery, and aimed to investigate the changes in the spindle generation before and after the surgery using low-density scalp EEG and electrical source imaging (ESI). METHODS: We analyzed N2-sleep EEGs from 19 children with DRE before and after surgery. We identified slow (8-12 Hz) and fast spindles (13-16 Hz), computed their spectral features and cortical generators through ESI and computed their distance from the EZ and irritative zone (IZ). We performed two-way ANOVA testing the effect of spindle type (slow vs. fast) and surgical phase (pre-surgery vs. post-surgery) on each feature. RESULTS: Power, frequency and cortical activation of slow spindles increased after surgery (p < 0.005), while this was not seen for fast spindles. Before surgery, the cortical generators of slow spindles were closer to the EZ (57.3 vs. 66.2 mm, p = 0.007) and IZ (41.3 vs. 55.5 mm, p = 0.02) than fast spindle generators. CONCLUSIONS: Our data indicate alterations in the EEG slow spindles after resective epilepsy surgery. Fast spindle generation on the contrary did not change after surgery. Although the study is limited by its retrospective nature, lack of healthy controls, and reduced cortical spatial sampling, our findings suggest a spatial relationship between the slow spindles and the epileptogenic generators.

Two-Stage Atomic Decomposition of Multichannel EEG and the Previously Undetectable Sleep Spindles.

We propose a two-step procedure for atomic decomposition of multichannel EEGs, based upon multivariate matching pursuit and dipolar inverse solution, from which atoms representing relevant EEG structures are selected according to prior knowledge. We detect sleep spindles in 147 polysomnographic recordings from the Montreal Archive of Sleep Studies. Detection is compared with human scorers and two state-of-the-art algorithms, which find only about a third of the structures conforming to the definition of sleep spindles and detected by the proposed method. We provide arguments supporting the thesis that the previously undetectable sleep spindles share the same properties as those marked by human experts and previously applied methods, and were previously omitted only because of unfavorable local signal-to-noise ratios, obscuring their visibility to both human experts and algorithms replicating their markings. All detected EEG structures are automatically parametrized by their time and frequency centers, width duration, phase, and spatial location of an equivalent dipolar source within the brain. It allowed us, for the first time, to estimate the spatial gradient of sleep spindles frequencies, which not only confirmed quantitatively the well-known prevalence of higher frequencies in posterior regions, but also revealed a significant gradient in the sagittal plane. The software used in this study is freely available.

Right-lateralized sleep spindles are associated with neutral over emotional bias in picture recognition: An overnight study.

Sleep is especially important for emotional memories, although the mechanisms for prioritizing emotional content are insufficiently known. As during waking, emotional processing during sleep may be hemispherically asymmetric; right-lateralized rapid-eye movement (REM) sleep theta (~4-7 Hz) is reportedly associated with emotional memory retention. No research exists on lateralized non-REM sleep oscillations. However, sleep spindles, especially when coupled with slow oscillations (SOs), facilitate off-line memory consolidation.Our primary goal was to examine how the lateralization (right-to-left contrast) of REM theta, sleep spindles, and SO-spindle coupling is associated with overnight recognition memory in a task consisting of neutral and emotionally aversive pictures. Thirty-two healthy adults encoded 150 target pictures before overnight sleep. The recognition of target pictures among foils (discriminability, d') was tested immediately, 12 hours, and 24 hours after encoding.Recognition discriminability between targets and foils was similar for neutral and emotional pictures in immediate and 12-h retrievals. After 24 hours, emotional pictures were less accurately discriminated (p < 0.001). Emotional difference at 24-h retrieval was associated with right-to-left contrast in frontal fast spindle density (p < 0.001). The lateralization of SO-spindle coupling was associated with higher neutral versus emotional difference across all retrievals (p = 0.004).Our findings contribute to a largely unstudied area in sleep-related memory research. Hemispheric asymmetry in non-REM sleep oscillations may contribute to how neutral versus emotional information is processed. This is presumably underlain by both mechanistic offline memory consolidation and a trait-like cognitive/affective bias that influences memory encoding and retrieval. Methodological choices and participants' affective traits are likely involved.

The adolescent pattern of sleep spindle development revealed by HD-EEG.

Sleep spindles are developmentally relevant cortical oscillatory patterns; however, they have mostly been studied by considering the entire spindle frequency range (11-15 Hz) without a distinction between the functionally and topographically different slow and fast spindles, using relatively few electrodes and analysing wide age-ranges. Here, we employ high-density night sleep electroencephalography in three age-groups between 12 and 20 years of age (30 females and 30 males) and analyse the adolescent developmental pattern of the four major parameters of slow and fast sleep spindles. Most of our findings corroborate those very few previous studies that also make a distinction between slow and fast spindles in their developmental analysis. We find spindle frequency increasing with age. A spindle density change is not obvious in our study. We confirm the declining tendencies for amplitude and duration, although within narrower, more specific age-windows than previously determined. Spindle frequency seems to be higher in females in the oldest age-group. Based on the pattern of our findings, we suggest that high-density electroencephalography, specifically targeting slow and fast spindle ranges and relatively narrow age-ranges would advance the understanding of both adolescent cortical maturation and development and the functional relevance of sleep spindles in general.

Electroencephalographic markers from routine sleep discriminate individuals who are vulnerable or resilient to sleep loss.

Sleep loss impairs cognition; however, individuals differ in their response to sleep loss. Current methods to identify an individual's vulnerability to sleep loss involve time-consuming sleep-loss challenges and neurobehavioural tests. Here, we sought to identify electroencephalographic markers of sleep-loss vulnerability obtained from routine night sleep. We retrospectively analysed four studies in which 50 healthy young adults (21 women) completed a laboratory baseline-sleep phase followed by a sleep-loss challenge. After classifying subjects as resilient or vulnerable to sleep loss, we extracted three electroencephalographic features from four channels during the baseline nights, evaluated the discriminatory power of these features using the first two studies (discovery), and assessed reproducibility of the results using the remaining two studies (reproducibility). In the discovery analysis, we found that, compared to resilient subjects, vulnerable subjects exhibited: (1) higher slow-wave activity power in channel O1 (p < 0.0042, corrected for multiple comparisons) and in channels O2 and C3 (p < 0.05, uncorrected); (2) higher slow-wave activity rise rate in channels O1 and O2 (p < 0.05, uncorrected); and (3) lower sleep spindle frequency in channels C3 and C4 (p < 0.05, uncorrected). Our reproducibility analysis confirmed the discovery results on slow-wave activity power and slow-wave activity rise rate, and for these two electroencephalographic features we observed consistent group-difference trends across all four channels in both analyses. The higher slow-wave activity power and slow-wave activity rise rate in vulnerable individuals suggest that they have a persistently higher sleep pressure under normal rested conditions.

Post-training sleep modulates motor adaptation and task-related beta oscillations.

Motor adaptation reflects the ability of the brain's sensorimotor system to flexibly deal with environmental changes to generate effective motor behaviour. Whether sleep contributes to the consolidation of motor adaptation remains controversial. In this study, we investigated the impact of sleep on motor adaptation and its neurophysiological correlates in a novel motor adaptation task that leverages a highly automatised motor skill, that is, typing. We hypothesised that sleep-associated memory consolidation would benefit motor adaptation and induce modulations in task-related beta band (13-30 Hz) activity during adaptation. Healthy young male experts in typing on the regular computer keyboard were trained to type on a vertically mirrored keyboard while brain activity was recorded using electroencephalography. Typing performance was assessed either after a full night of sleep with polysomnography or a similar period of daytime wakefulness. Results showed improved motor adaptation performance after nocturnal sleep but not after daytime wakefulness, and decreased beta power: (a) during mirrored typing as compared with regular typing; and (b) in the post-sleep versus the pre-sleep mirrored typing sessions. Furthermore, the slope of the electroencephalography signal, a measure of aperiodic brain activity, decreased during mirrored as compared with regular typing. Changes in the electroencephalography spectral slope from pre- to post-sleep mirrored typing sessions were correlated with changes in task performance. Finally, increased fast sleep spindle density (13-15 Hz) during the night following motor adaptation training was predictive of successful motor adaptation. These findings suggest that post-training sleep modulates neural activity supporting adaptive motor functions.

Sleep electroencephalography biomarkers of cognition in obstructive sleep apnea.

Obstructive sleep apnea has been associated with cognitive impairment and may be linked to disorders of cognitive function. These associations may be a result of intermittent hypoxaemia, sleep fragmentation and changes in sleep microstructure in obstructive sleep apnea. Current clinical metrics of obstructive sleep apnea, such as the apnea-hypopnea index, are poor predictors of cognitive outcomes in obstructive sleep apnea. Sleep microstructure features, which can be identified on sleep electroencephalography of traditional overnight polysomnography, are increasingly being characterized in obstructive sleep apnea and may better predict cognitive outcomes. Here, we summarize the literature on several major sleep electroencephalography features (slow-wave activity, sleep spindles, K-complexes, cyclic alternating patterns, rapid eye movement sleep quantitative electroencephalography, odds ratio product) identified in obstructive sleep apnea. We will review the associations between these sleep electroencephalography features and cognition in obstructive sleep apnea, and examine how treatment of obstructive sleep apnea affects these associations. Lastly, evolving technologies in sleep electroencephalography analyses will also be discussed (e.g. high-density electroencephalography, machine learning) as potential predictors of cognitive function in obstructive sleep apnea.

Reducing brain kynurenic acid synthesis precludes kynurenine-induced sleep disturbances.

Patients with neurocognitive disorders often battle sleep disturbances. Kynurenic acid is a tryptophan metabolite of the kynurenine pathway implicated in the pathology of these illnesses. Modest increases in kynurenic acid, an antagonist at glutamatergic and cholinergic receptors, result in cognitive impairments and sleep dysfunction. We explored the hypothesis that inhibition of the kynurenic acid synthesising enzyme, kynurenine aminotransferase II, may alleviate sleep disturbances. At the start of the light phase, adult male and female Wistar rats received systemic injections of either: (i) vehicle; (ii) kynurenine (100 mg kg-1 ; i.p.); (iii) the kynurenine aminotransferase II inhibitor, PF-04859989 (30 mg kg-1 ; s.c.); or (iv) PF-04859989 and kynurenine in combination. Kynurenine and kynurenic acid levels were evaluated in the plasma and brain. Separate animals were implanted with electroencephalogram and electromyogram telemetry devices to record polysomnography, and evaluate the vigilance states wake, rapid eye movement sleep and non-rapid eye movement sleep following each treatment. Kynurenine challenge increased brain kynurenic acid and resulted in reduced rapid eye movement sleep duration, non-rapid eye movement sleep delta power and sleep spindles. PF-04859989 reduced brain kynurenic acid formation when given prior to kynurenine, prevented disturbances in rapid eye movement sleep and sleep spindles, and enhanced non-rapid eye movement sleep. Our findings suggest that reducing kynurenic acid in conditions where the kynurenine pathway is activated may serve as a potential strategy for improving sleep dynamics.

An examination of sleep spindle metrics in the Sleep Heart Health Study: superiority of automated spindle detection over total sigma power in assessing age-related spindle decline.

BACKGROUND: Sleep spindle activity is commonly estimated by measuring sigma power during stage 2 non-rapid eye movement (NREM2) sleep. However, spindles account for little of the total NREM2 interval and therefore sigma power over the entire interval may be misleading. This study compares derived spindle measures from direct automated spindle detection with those from gross power spectral analyses for the purposes of clinical trial design. METHODS: We estimated spindle activity in a set of 8,440 overnight electroencephalogram (EEG) recordings from 5,793 patients from the Sleep Heart Health Study using both sigma power and direct automated spindle detection. Performance of the two methods was evaluated by determining the sample size required to detect decline in age-related spindle coherence with each method in a simulated clinical trial. RESULTS: In a simulated clinical trial, sigma power required a sample size of 115 to achieve 95% power to identify age-related changes in sigma coherence, while automated spindle detection required a sample size of only 60. CONCLUSIONS: Measurements of spindle activity utilizing automated spindle detection outperformed conventional sigma power analysis by a wide margin, suggesting that many studies would benefit from incorporation of automated spindle detection. These results further suggest that some previous studies which have failed to detect changes in sigma power or coherence may have failed simply because they were underpowered.

Sleep in 22q11.2 Deletion Syndrome: Current Findings, Challenges, and Future Directions.

PURPOSE OF REVIEW: To summarize current literature available on sleep in 22q11.2 Deletion Syndrome (22q11.2DS; Velocardiofacial or DiGeorge Syndrome), a neurogenetic disorder caused by a hemizygous deletion in a genomic region critical for neurodevelopment. Due to the greatly increased risk of developmental psychiatric disorders (e.g., autism and schizophrenia) in 22q11.2DS, this review focuses on clinical correlates of sleep disturbances and potential neurobiological underpinnings of these relationships. RECENT FINDINGS: Sleep disturbances are widely prevalent in 22q11.2DS and are associated with worse behavioral, psychiatric, and physical health outcomes. There are reports of sleep architecture and sleep neurophysiology differences, but the literature is limited by logistical challenges posed by objective sleep measures, resulting in small study samples to date. Sleep disturbances in 22q11.2DS are prevalent and have a substantial impact on well-being. Further investigation of sleep in 22q11.2DS utilizing multimodal sleep assessments has the potential to provide new insight into neurobiological mechanisms and a potential trans-diagnostic treatment target in 22q11.2DS.

Association of sleep and anaesthesia EEG biomarkers with preoperative MoCA score: A pilot study.

INTRODUCTION: Preoperative cognitive impairments increase the risk of postoperative complications. The electroencephalogram (EEG) could provide information on cognitive vulnerability. The feasibility and clinical relevance of sleep EEG (EEGsleep ) compared to intraoperative EEG (EEGintraop ) in cognitive risk stratification remains to be explored. We investigated similarities between EEGsleep and EEGintraop vis-a-vis preoperative cognitive impairments. METHODS: Pilot study including 27 patients (63 year old [53.5, 70.0]) to whom Montreal cognitive assessment (MoCA) and EEGsleep were administered 1 day before a propofol-based general anaesthesia, in addition to EEGintraop acquisition from depth-of-anaesthesia monitors. Sleep spindles on EEGsleep and intraoperative alpha-band power on EEGintraop were particularly explored. RESULTS: In total, 11 (41%) patients had a MoCA <25 points. These patients had a significantly lower sleep spindle power on EEGsleep (25 vs. 40 µv2 /Hz, p = .035) and had a weaker intraoperative alpha-band power on EEGintraop (85 vs. 150 µv2 /Hz, p = .001) compared to patients with normal MoCA. Correlation between sleep spindle and intraoperative alpha-band power was positive and significant (r = 0.544, p = .003). CONCLUSION: Preoperative cognitive impairment appears to be detectable by both EEGsleep and EEGintraop . Preoperative sleep EEG to assess perioperative cognitive risk is feasible but more data are needed to demonstrate its benefit compared to intraoperative EEG.

The effects of cognitive reappraisal and sleep on emotional memory formation.

Emotion regulation (i.e. either up- or down-regulating affective responses to emotional stimuli) has been shown to modulate long-term emotional memory formation. Further, research has demonstrated that the emotional aspects of scenes are preferentially remembered relative to neutral aspects (known as the emotional memory trade-off effect). This trade-off is often enhanced when sleep follows learning, compared to an equivalent period of time spent awake. However, the interactive effects of sleep and emotion regulation on emotional memory are poorly understood. We presented 87 participants with pictures of neutral or negative objects on neutral backgrounds paired with instructions to either increase or decrease their emotional response by altering personal relevance, or to passively view the stimuli. Following a 12 h period of sleep or wakefulness, participants were tested for their memory of objects and backgrounds separately. Although we replicated the emotional memory trade-off effect, no differences in the magnitude of the trade-off effect were observed between regulation conditions. Sleep improved all aspects of memory, but it did not preferentially benefit memory for emotional components of scenes. Irrespective of a period of sleep or wake following encoding, findings suggest emotion regulation during encoding did not influence memory for emotional items at a 12-hour delay.

Sleep Spindles Preferentially Consolidate Weakly Encoded Memories.

Sleep has been shown to be critical for memory consolidation, with some research suggesting that certain memories are prioritized for consolidation. Initial strength of a memory appears to be an important boundary condition in determining which memories are consolidated during sleep. However, the role of consolidation-mediating oscillations, such as sleep spindles and slow oscillations, in this preferential consolidation has not been explored. Here, 54 human participants (76% female) studied pairs of words to three distinct encoding strengths, with recall being tested immediately following learning and again 6 h later. Thirty-six had a 2 h nap opportunity following learning, while the remaining 18 remained awake throughout. Results showed that, across 6 h awake, weakly encoded memories deteriorated the fastest. In the nap group, however, this effect was attenuated, with forgetting rates equivalent across encoding strengths. Within the nap group, consolidation of weakly encoded items was associated with fast sleep spindle density during non-rapid eye movement sleep. Moreover, sleep spindles that were coupled to slow oscillations predicted the consolidation of weak memories independently of uncoupled sleep spindles. These relationships were unique to weakly encoded items, with spindles not correlating with memory for intermediate or strong items. This suggests that sleep spindles facilitate memory consolidation, guided in part by memory strength.SIGNIFICANCE STATEMENT Given the countless pieces of information we encode each day, how does the brain select which memories to commit to long-term storage? Sleep is known to aid in memory consolidation, and it appears that certain memories are prioritized to receive this benefit. Here, we found that, compared with staying awake, sleep was associated with better memory for weakly encoded information. This suggests that sleep helps attenuate the forgetting of weak memory traces. Fast sleep spindles, a hallmark oscillation of non-rapid eye movement sleep, mediate consolidation processes. We extend this to show that fast spindles were uniquely associated with the consolidation of weakly encoded memories. This provides new evidence for preferential sleep-based consolidation and elucidates a physiological correlate of this benefit.

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.