EEG Theta Power Research Articles

Increased subjective sleepiness and global EEG theta power during a post-night shift drive

Increased subjective sleepiness and global EEG theta power during a post-night shift drive

Sleep homeostatic pressure and PER3 VNTR gene polymorphism influence antidepressant response to sleep deprivation in bipolar depression

BackgroundCombined Total sleep deprivation (TSD) and light therapy (LT) cause a rapid improvement in bipolar depression which has been hypothesized to be paralleled by changes in sleep homeostasis. Recent studies showed that bipolar patients had lower changes of EEG theta power after sleep and responders to antidepressant TSD+LT slept less and showed a lower increase of EEG theta power then non-responders. A polymorphism in PER3 gene has been associated with diurnal preference, sleep structure and homeostatic response to sleep deprivation in healthy subjects. We hypothesized that the individual variability in the homeostatic response to TSD could be a correlate of antidepressant response and be influenced by genetic factors. MethodsWe administered three TSD+LT cycles to bipolar depressed patients. Severity of depression was rated on Hamilton Depression Rating Scale. Actigraphic recordings were performed in a group of patients. ResultsPER3 polymorphism influenced changes in total sleep time (F=2.24; p=0.024): while PER34/4 and PER34/5 patients showed a reduction in it after treatment, PER35/5 subjects showed an increase of about 40min, suggesting a higher homeostatic pressure. The same polymorphism influenced the change of depressive symptomatology during treatment (F=3.72; p=0.028). LimitationsSleep information was recorded till the day after the end of treatment: a longer period of observation could give more information about the possible maintenance of allostatic adaptation. ConclusionsA higher sleep homeostatic pressure reduced the antidepressant response to TSD+LT, while an allostatic adaptation to sleep loss was associated with better response. This process seems to be under genetic control.

Neural mechanisms of placebo anxiolysis.

The beneficial effects of placebo treatments on fear and anxiety (placebo anxiolysis) are well known from clinical practice, and there is strong evidence indicating a contribution of treatment expectations to the efficacy of anxiolytic drugs. Although clinically highly relevant, the neural mechanisms underlying placebo anxiolysis are poorly understood. In two studies in humans, we tested whether the administration of an inactive treatment along with verbal suggestions of anxiolysis can attenuate experimentally induced states of phasic fear and/or sustained anxiety. Phasic fear is the response to a well defined threat and includes attentional focusing on the source of threat and concomitant phasic increases of autonomic arousal, whereas in sustained states of anxiety potential and unclear danger requires vigilant scanning of the environment and elevated tonic arousal levels. Our placebo manipulation consistently reduced vigilance measured in terms of undifferentiated reactivity to salient cues (indexed by subjective ratings, skin conductance responses and EEG event-related potentials) and tonic arousal [indexed by cue-unrelated skin conductance levels and enhanced EEG alpha (8-12 Hz) activity], indicating a downregulation of sustained anxiety rather than phasic fear. We also observed a placebo-dependent sustained increase of frontal midline EEG theta (4-7 Hz) power and frontoposterior theta coupling, suggesting the recruitment of frontally based cognitive control functions. Our results thus support the crucial role of treatment expectations in placebo anxiolysis and provide insight into the underlying neural mechanisms.

Schema-conformant memories are preferentially consolidated during REM sleep

Memory consolidation is most commonly described by the standard model, which proposes an initial binding role for the hippocampus which diminishes over time as intracortical connections are strengthened. Recent evidence suggests that slow wave sleep (SWS) plays an essential role in this process. Existing animal and human studies have suggested that memories which fit tightly into an existing knowledge framework or schema might use an alternative consolidation route in which the medial prefrontal cortex takes on the binding role. In this study we sought to investigate the role of sleep in this process using a novel melodic memory task. Participants were asked to remember 32 melodies, half of which conformed to a tonal schema present in all enculturated listeners, and half of which did not fit with this schema. After a 24-h consolidation interval, participants were asked to remember a further 32 melodies, before being given a recognition test in which melodies from both sessions were presented alongside some previously unheard foils. Participants remembered schema-conformant melodies better than non-conformant ones. This was much more strongly the case for consolidated melodies, suggesting that consolidation over a 24-h period preferentially consolidated schema-conformant items. Overnight sleep was monitored between the sessions, and the extent of the consolidation benefit for schema-conformant items was associated with both the amount of REM sleep obtained and EEG theta power in frontal and central regions during REM sleep. Overall our data suggest that REM sleep plays a crucial role in the rapid consolidation of schema-conformant items. This finding is consistent with previous results from animal studies and the SLIMM model of Van Kesteren, Ruiter, Fernández, and Henson (2012), and suggest that REM sleep, rather than SWS, may be involved in an alternative pathway of consolidation for schema-conformant memories.

EEG theta and beta power spectra in adolescents with ADHD versus adolescents with ASD + ADHD.

Attention problems are common in youngsters with attention deficit hyperactivity disorder (ADHD) as well as in adolescents with combined autism spectrum disorder (ASD) and ADHD. However, it is unknown whether there is psychophysiological overlap and/or a difference in electroencephalogram (EEG) power spectra between ADHD and comorbid ASD and ADHD (ASD + ADHD), on and off stimulant medication. To explore potential differences and overlap, measures of theta and beta power in adolescents diagnosed with ADHD (n = 33) versus adolescents with combined ASD + ADHD (n = 20), categorized by stimulant medication use (57 % of the total sample), were compared. EEG measures were acquired in three conditions: (1) resting state, eyes closed (2) resting state, eyes open and (3) during an oddball task. In addition, performance on the d2 attention test was analyzed. Adolescents with ADHD displayed more absolute theta activity than adolescents with ASD + ADHD during the eyes open and task conditions, independent of stimulant medication use. In addition, only the adolescents with ADHD showed an association between diminished attention test performance and increased theta in the eyes open condition. Results of the current study suggest that although there is behavioral overlap between ADHD characteristics in adolescents with ADHD and adolescents with combined ASD + ADHD, the underlying psychophysiological mechanisms may be different. Adolescents with ASD + ADHD exhibited fewer of the EEG physiological signs usually associated with ADHD, although there was an overlap in attentional problems between the groups. This may indicate that treatments developed for ADHD work differently in some adolescents with ASD + ADHD and adolescents with ADHD only.

EEG Theta Power and Coherence to Octave Illusion in First-Episode Paranoid Schizophrenia with Auditory Hallucinations

Background: The exact mechanism behind auditory hallucinations in schizophrenia remains unknown. A corollary discharge dysfunction hypothesis has been put forward, but it requires further confirmation. Electroencephalography (EEG) of the Deutsch octave illusion might offer more insight, by demonstrating an abnormal cerebral activation similar to that under auditory hallucinations in schizophrenic patients. Methods: We invited 23 first-episode schizophrenic patients with auditory hallucinations and 23 healthy participants to listen to silence and two sound sequences, which consisted of alternating 400- and 800-Hz tones. EEG spectral power and coherence values of different frequency bands, including theta rhythm (3.5-7.5 Hz), were computed using 32 scalp electrodes. Task-related spectral power changes and task-related coherence differences were also calculated. Clinical characteristics of patients were rated using the Positive and Negative Syndrome Scale. Results: After both sequences of octave illusion, the task-related theta power change values of frontal and temporal areas were significantly lower, and the task-related theta coherence difference values of intrahemispheric frontal-temporal areas were significantly higher in schizophrenic patients than in healthy participants. Moreover, the task-related power change values in both hemispheres were negatively correlated and the task-related coherence difference values in the right hemisphere were positively correlated with the hallucination score in schizophrenic patients. Limitations: We only tested the Deutsch octave illusion in primary schizophrenic patients with acute first episode. Further studies might adopt other illusions or employ other forms of schizophrenia. Conclusion: Our results showed a lower activation but higher connection within frontal and temporal areas in schizophrenic patients under octave illusion. This suggests an oversynchronized but weak frontal area to exert an action to the ipsilateral temporal area, which supports the corollary discharge dysfunction hypothesis.

Listening to Mozart K.448 decreases electroencephalography oscillatory power associated with an increase in sympathetic tone in adults: a post-intervention study

SummaryObjectiveListening to Mozart K.448 has been demonstrated to improve spatial task scores, leading to what is known as the Mozart Effect. However, most of these reports only describe the phenomena but lack the scientific evidence needed to properly investigate the mechanism of Mozart Effect. In this study, we used electroencephalography (EEG) and heart rate variability (HRV) to evaluate the effects of Mozart K.448 on healthy volunteers to explore Mozart Effect.DesignAn EEG-based post-intervention analysis.SettingKaohsiung Medical University Hospital, Kaohsiung, Taiwan.ParticipantsTwenty-nine college students were enrolled. They received EEG and electrocardiogram examinations simultaneously before, during and after listening to the first movement of Mozart K.448.Main outcome measureEEG alpha, theta and beta power and HRV were compared in each stage.ResultsThe results showed a significant decrease in alpha, theta and beta power when they listened to Mozart K.448. In addition, the average root mean square successive difference, the proportion derived by dividing NN50 by the total number of NN intervals, standard deviations of NN intervals and standard deviations of differences between adjacent NN intervals showed a significant decrease, while the high frequency revealed a significant decrease with a significantly elevated low-frequency/high-frequency ratio.ConclusionListening to Mozart K.448 significantly decreased EEG alpha, theta and beta power and HRV. This study indicates that there is brain cortical function and sympathetic tone activation in healthy adults when listening to Mozart K.448, which may play an important role in the mechanism of Mozart Effect.

Longitudinal study of EEG frequency maturation and power changes in children on the Russian North

The aim of the study was to reveal longitudinal changes in electroencephalogram spectral power and frequency (percentage frequency composition of EEG and alpha peak frequency) patterns in normal children from northern Russia. Fifteen children (9 girls and 6 boys) participated in the study. The resting state (eyes closed) EEGs were recorded yearly (2005–2013) from age 8 to age 16–17 for each child. EEG frequency patterns were estimated as the percentages of waves with a 1Hz step revealed by measuring the interval durations between points crossing zero (isoline) by a curve. EEG spectral power changes were analyzed for delta (1.5–4Hz), theta (4–7.5Hz), alpha-1 (7.5–9.5Hz), alpha-2 (9.5–12.5Hz), beta-1 (12.5–18Hz) and beta-2 (18–30Hz) bands. According to the frequency composition of the EEG signals fast synchronous, polymorphous synchronous, polymorphous desynchronous and slow synchronous types of children EEG were revealed. These EEG types were relatively stable during adolescence. In these EEG types, the frequency patterns and spectral power dynamics with age had several common and specific features. Slow wave percentage and spectral power in the delta band remarkably decreased with age in all groups. Starting from the theta band the EEG types were characterized by different EEG spectral power changes with age. In fast synchronous EEG type, the theta and alpha-1 EEG power decreased, and the alpha-2 power increased in the occipital and parietal areas. The polymorphous synchronous type was characterized by increased both the alpha-1 and alpha-2 power with regional peculiarities. In the polymorphous desynchronous type spectral power in all bands decreased with age, and in the slow synchronous type, the alpha-1 power massively increased with age. Obtained results suggest predictive strength of the spatial-frequency patterns in EEG for its following maturation through the years.

Genetic variability in the human cannabinoid receptor 1 is associated with resting state EEG theta power in humans

It has long been postulated that exogenous cannabinoids have a profound effect on human cognitive functioning. These cannabinoid effects are thought to depend, at least in parts, on alterations of phase-locking of local field potential neuronal firing. The latter can be measured as activity in the theta frequency band (4–7Hz) by electroencephalogram. Theta oscillations are supposed to serve as a mechanism in neural representations of behaviorally relevant information. However, it remains unknown whether variability in endogenous cannabinoid activity is involved in theta rhythms and therefore, may serve as an individual differences index of human cognitive functioning. To clarify this issue, we recorded resting state EEG activity in 164 healthy human subjects and extracted EEG power across frequency bands (δ, θ, α, and β). To assess variability in the endocannabinoid system, two genetic polymorphisms (rs1049353, rs2180619) within the cannabinoid receptor 1 (CB1) were determined in all participants. As expected, we observed significant effects of rs1049353 on EEG power in the theta band at frontal, central and parietal electrode regions. Crucially, these effects were specific for the theta band, with no effects on activity in the other frequency bands. Rs2180619 showed no significant associations with theta power after Bonferroni correction. Taken together, we provide novel evidence in humans showing that genetic variability in the cannabinoid receptor 1 is associated with resting state EEG power in the theta frequency band. This extends prior findings of exogenous cannabinoid effects on theta power to the endogenous cannabinoid system.

Stimulus-response mappings shape inhibition processes: a combined EEG-fMRI study of contextual stopping.

Humans are rarely faced with one simple task, but are typically confronted with complex stimulus constellations and varying stimulus-relevance in a given situation. Through modifying the prototypical stop-signal task and by combined recording and analysis of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI), we studied the effects of stimulus relevance for the generation of a response or its inhibition. Stimulus response mappings were modified by contextual cues, indicating which of two different stimuli following a go stimulus was relevant for stopping. Overall, response inhibition, that is comparing successful stopping to a stop-signal against go-signal related processes, was associated with increased activity in right inferior and left midfrontal regions, as well as increased EEG delta and theta power; however, stimulus-response conditions in which the most infrequent stop-signal was relevant for inhibition, were associated with decreased activity in regions typically involved in response inhibition, as well as decreased activity in the delta and theta bands as compared to conditions wherein the relevant stop-signal frequency was higher. Behaviorally, this (aforementioned) condition, which demanded inhibition only from the most infrequent stimulus, was also associated with reduced reaction times and lower error rates. This pattern of results does not align with typical stimulus frequency-driven findings and suggests interplay between task relevance and stimulus frequency of the stop-signal. Moreover, with a multimodal EEG-fMRI analysis, we demonstrated significant parameterization for response inhibition with delta, theta and beta time-frequency values, which may be interpreted as reflecting conflict monitoring, evaluative and/or motor processes as suggested by previous work (Huster et al., 2013; Aron, 2011). Further multimodal results suggest a possible neurophysiological and behavioral benefit under conditions whereby the most infrequent stimulus demanded inhibition, indicating that the frequency of the stop-signal interacts with the current stimulus-response contingency. These results demonstrate that response inhibition is prone to influence from other cognitive functions, making it difficult to dissociate real inhibitory capabilities from the influence of moderating mechanisms.

Genetic overlap between ADHD symptoms and EEG theta power

Biological markers that are grounded in neuroscience may facilitate understanding of the pathophysiology of complex psychiatric disorders. One of the most consistent and robust neural abnormalities in attention deficit hyperactivity disorder (ADHD) is increased EEG power in the theta band at rest (4–8Hz). The present study used a twin design to estimate the extent of genetic overlap between increased theta power and risk for ADHD in order to validate theta power as a marker of genetic risk for ADHD. At rest, EEG was measured in 30 monozygotic and dizygotic adolescent twin pairs concordant or discordant for high ADHD symptom scores and 37 monozygotic and dizygotic control twin pairs with low ADHD symptom scores. Structural equation modelling was used to estimate the heritability of theta power and partition the genetic and environmental contributions to the overlap between ADHD and theta power. A significant phenotypic correlation between ADHD symptoms and elevated theta power was found. Theta power demonstrated moderate to high heritability estimates (0.77) and moderate genetic correlations with ADHD (0.35) suggesting shared genetic influences. Increased theta power is a candidate biological marker of genetic risk for ADHD, which warrants further investigation of the neurobiological mechanisms that underlie the genetic relationship.

Preparation for action: psychophysiological activity preceding a motor skill as a function of expertise, performance outcome, and psychological pressure.

Knowledge of the psychophysiological responses that characterize optimal motor performance is required to inform biofeedback interventions. This experiment compared cortical, cardiac, muscular, and kinematic activity in 10 experts and 10 novices as they performed golf putts in low- and high-pressure conditions. Results revealed that in the final seconds preceding movement, experts displayed a greater reduction in heart rate and EEG theta, high-alpha, and beta power, when compared to novices. EEG high-alpha power also predicted success, with participants producing less high-alpha power in the seconds preceding putts that were holed compared to those that were missed. Increased pressure had little impact on psychophysiological activity. It was concluded that greater reductions in EEG high-alpha power during preparation for action reflect more resources being devoted to response programming, and could underlie successful accuracy-based performance.

Athletes in a Slump: Neurophysiological Evidence from Frontal Theta Activity

The purpose of this study is to investigate the neurophysiological differences in athletes who suffer from a slump and other athletes who do not. Eighteen high school student athletes participated in this experiment. A subjective questionnaire was conducted to identify athletes in a slump (i.e., the slump group) and not in a slump (i.e., the no-slump group). EEG data was recorded at 4 regions (left prefrontal, right prefrontal, left frontal, and right frontal). A two-way (2 groups x 4 regions) ANOVA was performed on the dependent variable (i.e., frontal theta power). The findings of this study demonstrated that participants in the no-slump group showed higher frontal theta activity than their counterparts in the slump group. From the findings of this study, it is suggested that mental fatigue may cause low frontal theta activity in athletes who experience a slump. The present study makes an important contribution to the current literature by being the first to report that EEG theta power over frontal regions can be used as a marker of athletes suffering from a slump.

EPA-1603 - Changes of resting-state eeg and functional connectivity in the sensor and source space of patients with major depression

Introduction Dyfunctions of prefrontal neuronal circuits contribute to the pathophysiology of depression. Previous studies showed increased functional MRI and EEG connectivity in patients with depression. In this study we investigated a large sample of patients with major depression (n=228) and healthy subjects (n=215). Methods Spectrotemporal dynamics during resting state with closed eyes were analyzed in sensor and source space to examine functional EEG connectivity (fcEEG) alterations between groups. Quantitative measures of delta, theta, alpha, beta and gamma power, hemispheric asymmetry, coherence, phase and current source density (CSD, eLORETA) analyses were calculated from artifact-free EEG recordings. Results EEG theta power was increased in all brain regions in the group of patients with a focus in frontal regions and increased frontal theta and alpha power. Excessive coherence differences were detected in the delta, theta and alpha-bands in frontal, frontal-temporal and frontal-parietal regions. There were changes in phase differences in the delta, theta, alpha-bands between patients and healthy subjects. Differences in CSD were found for the delta, theta, alpha-band in the (rostral and subgenual) anterior cingulate cortex (ACC) with increased CSD in the patients. Conclusion The main finding of the present study was an increase in cortical slow-wave activity in sensor and source space in patients with depression revealing marked differences in prefrontal cortical networks. Functional delta, theta and alpha connectivity (coherence and phase) were altered with a predominance in the left hemisphere. Dysfunctions of the ACC, together with alterations in fcEEG may contribute to the pathophysiology of major depression.

Melatonin reverts signs of aging in the sleep of rats

Introduction Two basic properties summarize the biological effects of melatonin: the antioxidant properties and its activity as a marker of biological time. Both effects may counteract the deleterious consequences of aging. First, the cellular damage caused by free radicals has been claimed as a factor to explain many effects of aging. In addition, aged individuals suffer important perturbations in their sleep and biological rhythms. Both effects coincide with the practical suppression of melatonin secretion in aged individuals, a fact suggesting the therapeutic effectiveness of melatonin to revert the consequences of aging. The present study aims at recording the effects of melatonin administration to revert the effects of age in the sleep of rats. Materials and methods Wistar young and old rats (3 and 24 months, respectively, at the beginning of experiments) were used for the study. Two weeks before starting treatment, each animal was surgically implanted with two monopolar electrodes in the surface of the cortex for EEG recording and two bipolar EMG electrodes in the neck muscles for EMG. EOG electrodes were not used. Instead, REM sleep was identified by the presence of theta waves in the EEG and eye movements were monitorized through a closed video system. After recovery, the rats were housed individually and received ad libitum food. For drinking, old rats of the experimental group received melatonin dissolved in ethanol and then diluted in water in a proportion of 2%. The melatonin contents was calculated to provide an approximate daily dose of 1 mg/k bw during 30 days. The volume of consumed liquid was recorded every day and the proportions were corrected accordingly to maintain the desired dosage. Young and old control animals only received the 2% ethanol/water mixture. After 30 days of melatonin administration, the sleep of the rats was recorded during two hours (12:00–14:00). Samples of the recordings were selected corresponding to unambiguous waking, NREM and REM stages avoiding artifacts. The EEG recordings were submitted to Fourier analysis to obtain the power in the four typical frequency ranges. Results Aged control rats showed a significant reduction in delta and theta EEG power when compared to young controls. Melatonin administered to the experimental group reverted the changes, increasing delta and theta power during NREM and NREM, respectively. No significant changes were observed in waking. These results suggest the effectiveness of exogenous melatonin administration to correct the sleep perturbations observed in aged individuals. Conclusion Chronic low doses of melatonin improve the sleep quality in aging rats.

Sleep phenotype characterization of peripheral and central mouse models of myotonic dystrophy

Excessive daytime sleepiness and associated alterations in REM sleep patterns are among the most characteristic non-muscular features of myotonic dystrophy (DM). The symptoms of DM are caused by an expanded C (C) UG repeat that sequesters muscleblind-like protein 1 (MBNL1) and MBNL2, proteins that regulates alternative splicing required for fetal to adult developments. A recent study strongly suggests that major pathological changes in the DM brain are attributable to MBNL2 sequestration by toxic RNAs and dysregulation of specific alternative splicing events required for normal adult CNS function. We thus performed sleep EEG/EMG evaluations on Mbnl1 and Mbnl2 knockout (KO) mice. Adult wild and KO mice of Mbnl1 or Mbnl2 at 6 month of age (Mbnl1; n = 7, Mbnl2; n = 8) were implanted with EEG and EMG electrodes along with E-mitters. Sleep deprivation was performed for 6 h after one full day of baseline by gentle handling. Mbnl1 and Mbnl2 KOs had normal amounts, and natural diurnal distributions, of wakefulness and NREM sleep in the 12:12 LD condition. Shorter sleep latency and modest wake fragmentation during dark periods (frequent/shorter wake episodes) were observed in the Mbnl2 KO mice. However, the most profound sleep phenotypes observed in the Mbnl2 KO mice were an increase in REM sleep amounts, associated with increased numbers of REM sleep episodes, and increased EEG theta power. This change was most notable during the dark/active period. No direct transition from Wake to REM sleep, an EEG/EMG phenotype equivalent to behavioral cataplexy, was seen in either WT or Mbnl2 KO mice. A change in REM sleep in Mbnl2 KOs was also observed during rebound sleep after a 6-h sleep deprivation period initiated at ZT 0, where a more profound REM sleep rebound was observed in Mbnl2 KO mice, compared to WT mice. These REM specific changes were not observed in the Mbnl1 KO mice. Our results indicate that Mbnl2, but not Mbnl1, KO mice exhibit increased REM sleep propensity, suggesting REM-associated sleep abnormality in Mbnl2 KO are caused by dysregulation of specific alternative splicing events in the brain, and this may be one of the most important sleep abnormalities in DM. REM sleep characteristics in DM might be a residual of infant-type REM sleep, as infants of altricial species, including human and mice, spend large majority of time in REM sleep.

Optogenetic and pharmacogenetic probing of rapid eye movement (REM) sleep circuitry

Introduction Rapid eye movement (REM) sleep is characterized by the activation of cortical electroencephalogram (EEG) and loss of muscle tone (atonia). The exact neuronal circuit mediating the generation and timing of this state is not fully understood. The subcoeruleus (Sub-C) neurons are hypothesized to generate REM sleep and its characteristics. Here we aimed to determine how optogenetics and pharmacogenetic stimulation impacts REM sleep expression. Materials and methods Study#1: To precisely control the neuronal activity of the Sub-C region, we bilaterally infused 200 nL of an adeno-associated viral vector (AAV) containing a light-sensitive opsin (AAV-hsyn- hChR2(H134R)-eYFP) virus into the Sub-C of 4 mice. Animals were instrumented for EEG and EMG recordings. Neurons were stimulated with short blue light pulses (5 ms) at 1 and 10 Hz either independently of behavioral state or specifically during REM sleep. Study#2: To stimulate the Sub-C population for longer time periods, we bilaterally microinjected 400 nL of an AAV harboring a modified muscarinic G-protein coupled receptor (AAV-HSYN-HA-hm3D(Gq)- IRES-mCitrine) into the Sub-C of 3 mice. Administration of clozapine-N-oxide (CNO, 5 mg/kg) activated neurons in the Sub-C. Only animals that had histological verification of ChR2 and hm3D(Gq) receptor expression in the Sub-C region were used for analysis. Results We found that semi-chronic bilateral light activation of Sub-C neurons at 10 Hz, but not 1 Hz, triggered REM sleep-like EEG activity (theta, 4–8 Hz) during light stimulation, and increased EEG Theta power by 64 ± 16% compared to baseline. Under some conditions, light stimulation prolonged the duration of REM sleep episodes by almost 2-fold. Pharmacogenetic manipulation of the neurons in the Sub-C caused a change in behavioural phenotype where the distribution of EEG frequencies shifted towards a REM sleep-like pattern (theta, 4–8 Hz) independent of the behavioural state. Moreover, the average duration of REM sleep-like periods were greater than REM sleep periods under control condition (i.e., saline). Conclusion These results support the hypothesis that the Sub-C region is involved in controlling REM sleep and its associated phenomena. Acknowledgements This research was funded by the Natural Sciences and Engineering Research Council of Canada (NSERC) , the Canadian Institutes of Health Research (CIHR) and the CIHR Sleep and Biological Rhythms Toronto .

Neuronal oscillations and functional interactions between resting state networks.

Functional magnetic imaging (fMRI) studies showed that resting state activity in the healthy brain is organized into multiple large-scale networks encompassing distant regions. A key finding of resting state fMRI studies is the anti-correlation typically observed between the dorsal attention network (DAN) and the default mode network (DMN), which - during task performance - are activated and deactivated, respectively. Previous studies have suggested that alcohol administration modulates the balance of activation/deactivation in brain networks, as well as it induces significant changes in oscillatory activity measured by electroencephalography (EEG). However, our knowledge of alcohol-induced changes in band-limited EEG power and their potential link with the functional interactions between DAN and DMN is still very limited. Here we address this issue, examining the neuronal effects of alcohol administration during resting state by using simultaneous EEG-fMRI. Our findings show increased EEG power in the theta frequency band (4-8 Hz) after administration of alcohol compared to placebo, which was prominent over the frontal cortex. More interestingly, increased frontal tonic EEG activity in this band was associated with greater anti-correlation between the DAN and the frontal component of the DMN. Furthermore, EEG theta power and DAN-DMN anti-correlation were relatively greater in subjects who reported a feeling of euphoria after alcohol administration, which may result from a diminished inhibition exerted by the prefrontal cortex. Overall, our findings suggest that slow brain rhythms are responsible for dynamic functional interactions between brain networks. They also confirm the applicability and potential usefulness of EEG-fMRI for central nervous system drug research.

INDIVIDUAL PRECONSCIOUS AFFECTIVE BIASES TO THREATENING AND APPETITIVE FACIAL STIMULI AND CARDIOVASCULAR STRESS-REACTIVITY

To investigate cardiovascular stress-reactivity in association with individual preconscious affective biases to threatening and appetitive facial stimuli. Preconscious affective biases were assessed in healthy individuals (n = 38, mean age 28, 10 years, 1SD = 8.64) using a modified (masked) version of a pictorial emotional Stroop task (backward masking of the angry, fearful and joyful faces). It was revealed that individual preconscious bias to speeded up perception of angry faces correlates significantly with heightened anxiety, lowered platelet serotonin (5-HT) levels, sustained central overactivation of at rest (as indexed by lowered delta, theta, and beta-1 EEG power over frontal, central and posterior cortical areas) and exaggerated arterial blood pressure stress-reactivity during re-experiencing of personally relevant anger. considering uncovered associations, individuals with preconscious bias to speeded up perception of angry faces may be regarded as having enhanced risk to fall sick with essential hypertension, yet this perceptive bias could be seen as a putative neurobehavioral predictor of the risk.

The glycolytic metabolite methylglyoxal induces changes in vigilance by generating low-amplitude non-REM sleep

Methylglyoxal (MG), an essential by-product of glycolysis, is a highly reactive endogenous α-oxoaldehyde. Although high levels of MG are cytotoxic, physiological doses of MG were shown to reduce anxiety-related behavior through selective activation of γ-aminobutyric acid type A (GABAA) receptors. Because the latter play a major role in sleep induction, this study examined the potential of MG to regulate sleep. Specifically, we assessed how MG influences sleep-wake behavior in CD1 mice that received intracerebroventricular injections of either vehicle or 0.7 µmol MG at onset of darkness. We used electroencephalogram (EEG) and electromyogram (EMG) recordings to monitor changes in vigilance states, sleep architecture and the EEG spectrum, for 24 h after receipt of injections. Administration of MG rapidly induced non-rapid eye movement sleep (NREMS) and, concomitantly, decreased wakefulness and suppressed EEG delta power during NREMS. In addition, MG robustly enhanced the amount and number of episodes of an unclassified state of vigilance in which EMG, as well as EEG delta and theta power, were very low. MG did not affect overall rapid eye movement sleep (REMS) in a given 24-h period, but significantly reduced the power of theta activity during REMS. Our results provide the first evidence that MG can exert sleep-promoting properties by triggering low-amplitude NREMS.