Increased Gamma Power Research Articles

Negative Allosteric Modulation of Gamma-Aminobutyric Acid A Receptors at α5 Subunit–Containing Benzodiazepine Sites Reverses Stress-Induced Anhedonia and Weakened Synaptic Function in Mice

BackgroundAbnormal reward processing, typically anhedonia, is a hallmark of human depression and is accompanied by altered functional connectivity in reward circuits. Negative allosteric modulators of GABAA (gamma-aminobutyric acid A) receptors (GABA-NAMs) have rapid antidepressant-like properties in rodents and exert few adverse effects, but molecular targets underlying their behavioral and synaptic effects remain undetermined. We hypothesized that GABA-NAMs act at the benzodiazepine site of GABAA receptors containing α5 subunits to increase gamma oscillatory activity, strengthen synapses in reward circuits, and reverse anhedonia. MethodsAnhedonia was induced by chronic stress in male mice and assayed by preferences for sucrose and female urine (n = 5–7 mice/group). Hippocampal slices were then prepared for electrophysiological recording (n = 1–6 slices/mouse, 4–6 mice/group). Electroencephalography power was quantified in response to GABA-NAM and ketamine administration (n = 7–9 mice/group). ResultsChronic stress reduced sucrose and female urine preferences and hippocampal temporoammonic-CA1 synaptic strength. A peripheral injection of the GABA-NAM MRK-016 restored hedonic behavior and AMPA-to-NMDA ratios in wild-type mice. These actions were prevented by pretreatment with the benzodiazepine site antagonist flumazenil. MRK-016 administration increased gamma power over the prefrontal cortex in wild-type mice but not α5 knockout mice, whereas ketamine promoted gamma power in both genotypes. Hedonic behavior and AMPA-to-NMDA ratios were only restored by MRK-016 in stressed wild-type mice but not α5 knockout mice. Conclusionsα5-Selective GABA-NAMs exert rapid anti-anhedonic actions and restore the strength of synapses in reward regions by acting at the benzodiazepine site of α5-containing GABAA receptors. These results encourage human studies using GABA-NAMs to treat depression by providing readily translatable measures of target engagement.

The hippocampus as the switchboard between perception and memory

Adaptive memory recall requires a rapid and flexible switch from external perceptual reminders to internal mnemonic representations. However, owing to the limited temporal or spatial resolution of brain imaging modalities used in isolation, the hippocampal-cortical dynamics supporting this process remain unknown. We thus employed an object-scene cued recall paradigm across two studies, including intracranial electroencephalography (iEEG) and high-density scalp EEG. First, a sustained increase in hippocampal high gamma power (55 to 110 Hz) emerged 500 ms after cue onset and distinguished successful vs. unsuccessful recall. This increase in gamma power for successful recall was followed by a decrease in hippocampal alpha power (8 to 12 Hz). Intriguingly, the hippocampal gamma power increase marked the moment at which extrahippocampal activation patterns shifted from perceptual cue toward mnemonic target representations. In parallel, source-localized EEG alpha power revealed that the recall signal progresses from hippocampus to posterior parietal cortex and then to medial prefrontal cortex. Together, these results identify the hippocampus as the switchboard between perception and memory and elucidate the ensuing hippocampal-cortical dynamics supporting the recall process.

Resting‐state EEG gamma power and coherence might be an indicator of hyperexitability in patients with early‐onset Alzheimer’s disease

AbstractBackgroundEarly‐onset Alzheimer’s disease (EOAD) is characterized by disease onset age (<65 years) and non‐amnestic symptoms at the initial stage. Disease course is different from the late‐onset AD (LOAD) in terms of pathology, neuropsychological manifestations and topography of electrophysiological changes. Present study aims to investigate resting state gamma power and connectivity changes in patients with EOAD compared to healthy controls.MethodThe study included 24 individuals with CSF‐proven EOAD (who met the NIA‐AA diagnostic criteria, McKhann et al., 2011) and demographically matched 24 healthy controls. Four minutes of eyes closed resting state EEG was recorded. Artifact‐free six‐second epochs were obtained. Power and coherency were measured for the total gamma (30–48Hz), gamma‐1 (30‐35Hz), gamma‐2 (36‐40Hz), and gamma‐3 (41‐48Hz). Imaginary part of coherency (ICoh) and maximum absolute values were calculated for intra‐hemispheric, inter‐hemispheric and midline electrode pairs.ResultFFT analysis showed higher gamma‐2 [F(1,46)=4,732,p=0.032], and gamma‐3 [F(1,46)=4,158,p=0.047] power in the EOAD group compared to controls. In the coherence analysis, the EOAD group had higher gamma‐2 inter‐hemispheric ICoh values than controls [F(1,46)=5.473;p=0.024]. The total intra‐hemispheric gamma values of the EOAD group were higher in the F8‐TP8 pair, but lower in the P8‐O2 and F4‐C4 pairs compared to controls [F(11,506)=1.901;p=0.037]. Intra‐hemispheric gamma‐2 values of the EOAD group were higher in the F8‐TP8 pair, but lower in the C3‐O1 pair [F(11,506)=2.207;p=0.031]. Midline gamma‐1 ICoh values were lower in the EOAD group than controls [F(1.46)=8.352;p=0.006].ConclusionTo our knowledge this is the first study to examine resting state gamma changes in individuals with CSF proven EOAD. Increased gamma power and connectivity in patients with LOAD (Başar et al., 2016,2017; van Deursen et al., 2008,2011) and Parkinson’s disease dementia (Pal et al., 2020) were reported. Increased power and connectivity were thought to reflect shared tau pathology between brain regions (Franzmeier et al., 2019). Literature provides evidence for hyperexcitability due to increased glutamate in AMPA and NMDA receptors in patients with AD (Um et al., 2012). Our results from CSF‐proven EOAD patients suggest that gamma power and connectivity might be good indicators of hyperexcitability in AD.

Identifying the neurophysiological effects of memory-enhancing amygdala stimulation using interpretable machine learning

BackgroundDirect electrical stimulation of the amygdala can enhance declarative memory for specific events. An unanswered question is what underlying neurophysiological changes are induced by amygdala stimulation. ObjectiveTo leverage interpretable machine learning to identify the neurophysiological processes underlying amygdala-mediated memory, and to develop more efficient neuromodulation technologies. MethodPatients with treatment-resistant epilepsy and depth electrodes placed in the hippocampus and amygdala performed a recognition memory task for neutral images of objects. During the encoding phase, 160 images were shown to patients. Half of the images were followed by brief low-amplitude amygdala stimulation. For local field potentials (LFPs) recorded from key medial temporal lobe structures, feature vectors were calculated by taking the average spectral power in canonical frequency bands, before and after stimulation, to train a logistic regression classification model with elastic net regularization to differentiate brain states. ResultsClassifying the neural states at the time of encoding based on images subsequently remembered versus not-remembered showed that theta and slow-gamma power in the hippocampus were the most important features predicting subsequent memory performance. Classifying the post-image neural states at the time of encoding based on stimulated versus unstimulated trials showed that amygdala stimulation led to increased gamma power in the hippocampus. ConclusionAmygdala stimulation induced pro-memory states in the hippocampus to enhance subsequent memory performance. Interpretable machine learning provides an effective tool for investigating the neurophysiological effects of brain stimulation.

Anterior thalamic stimulation improves working memory precision judgments

BackgroundThe anterior nucleus of thalamus (ANT) has been suggested as an extended hippocampal system. The circuit of ANT and hippocampus has been widely demonstrated to be associated with memory function. Both lesions to each region and disrupting inter-regional information flow can induce working memory impairment. However, the role of this circuit in working memory precision remains unknown. ObjectiveTo test the role of the hippocampal-anterior thalamic pathway in working memory precision, we delivered intracranially electrical stimulation to the ANT. We hypothesize that ANT stimulation can improve working memory precision. MethodsPresurgical epilepsy patients with depth electrodes in ANT and hippocampus were recruited to perform a color-recall working memory task. Participants were instructed to point out the color they were supposed to recall by clicking a point on the color wheel, while the intracranial EEG data were synchronously recorded. For randomly selected half trials, a bipolar electrical stimulation was delivered to the ANT electrodes. ResultsWe found that compared to non-stimulation trials, working memory precision judgements were significantly improved for stimulation trials. ANT electrical stimulation significantly increased spectral power of gamma (30–100 Hz) oscillations and decreased interictal epileptiform discharges (IED) in the hippocampus. Moreover, the increased gamma power during the pre-stimulus and retrieval period predicted the improvement of working memory precision judgements. ConclusionANT electrical stimulation can improve working memory precision judgements and modulate hippocampal gamma activity, providing direct evidence on the role of the human hippocampal-anterior thalamic axis in working memory precision.

Understanding the neurological mechanism involved in enhanced memory recall task following binaural beat: a pilot study

Binaural beat (BB) is a promising technique for memory improvement in elderly or people with neurological conditions. However, the related modulation of cortical networks followed by behavioral changes has not been investigated. The objective of this study is to establish a relationship between BB oscillatory brain activity evoked by stimulation and a behavioral response in a short term memory task. Three Groups A, B, and C of 20 participants each received alpha (10 Hz), beta (14 Hz), and gamma (30 Hz) BB, respectively, for 15 min. Their EEG was recorded in pre, during, and post BB states. Participants performed a digit span test before and after a BB session. A significant increase in the cognitive score was found only for Group A while a significant decrease in reaction time was noted for Groups A and C. Group A had a significant decrease of theta and increase of alpha power, and a significant increase of theta and decrease of gamma imaginary coherence (ICH) post BB. Group C had a significant increase in theta and gamma power accompanied by the increase of theta and gamma ICH post BB. The effectiveness of BB depends on the frequency of stimulation. A putative neural mechanism involves an increase in theta ICH in parieto-frontal and interhemispheric frontal networks.

Ketamine Alters Functional Gamma and Theta Resting-State Connectivity in Healthy Humans: Implications for Schizophrenia Treatment Targeting the Glutamate System.

Disturbed functional connectivity is assumed to cause neurocognitive deficits in patients suffering from schizophrenia. A Glutamate N-methyl-D-aspartate receptor (NMDAR) dysfunction has been suggested as a possible mechanism underlying altered connectivity in schizophrenia, especially in the gamma- and theta-frequency range. The present study aimed to investigate the effects of the NMDAR-antagonist ketamine on resting-state power, functional connectivity, and schizophrenia-like psychopathological changes in healthy volunteers. In a placebo-controlled crossover design, 25 healthy subjects were recorded using resting-state 64-channel-electroencephalography (EEG) (eyes closed). The imaginary coherence-based Multivariate Interaction Measure (MIM) was used to measure gamma and theta connectivity across 80 cortical regions. The network-based statistic was applied to identify involved networks under ketamine. Psychopathology was assessed with the Positive and Negative Syndrome Scale (PANSS) and the 5-Dimensional Altered States of Consciousness Rating Scale (5D-ASC). Ketamine caused an increase in all PANSS (p < 0.001) as well as 5D-ASC scores (p < 0.01). Significant increases in resting-state gamma and theta power were observed under ketamine compared to placebo (p < 0.05). The source-space analysis revealed two distinct networks with an increased mean functional gamma- or theta-band connectivity during the ketamine session. The gamma-network consisted of midline regions, the cuneus, the precuneus, and the bilateral posterior cingulate cortices, while the theta-band network involved the Heschl gyrus, midline regions, the insula, and the middle cingulate cortex. The current source density (CSD) within the gamma-band correlated negatively with the PANSS negative symptom score, and the activity within the gamma-band network correlated negatively with the subjective changed meaning of percepts subscale of the 5D-ASC. These results are in line with resting-state patterns seen in people who have schizophrenia and argue for a crucial role of the glutamate system in mediating dysfunctional gamma- and theta-band-connectivity in schizophrenia. Resting-state networks could serve as biomarkers for the response to glutamatergic drugs or drug development efforts within the glutamate system.

EEG and Sleep Effects of Tramadol Suggest Potential Antidepressant Effects with Different Mechanisms of Action.

Tramadol is a widely used, centrally acting, opioid analgesic compound, with additional inhibitory effects on the synaptic reuptake of serotonin and noradrenaline, as well as on the 5-HT2 and NMDA receptors. Preclinical and clinical evidence also suggests its therapeutic potential in the treatment of depression and anxiety. The effects of most widely used antidepressants on sleep and quantitative electroencephalogram (qEEG) are well characterized; however, such studies of tramadol are scarce. Our aim was to characterize the effects of tramadol on sleep architecture and qEEG in different sleep–wake stages. EEG-equipped Wistar rats were treated with tramadol (0, 5, 15 and 45 mg/kg) at the beginning of the passive phase, and EEG, electromyogram and motor activity were recorded. Tramadol dose-dependently reduced the time spent in rapid eye movement (REM) sleep and increased the REM onset latency. Lower doses of tramadol had wake-promoting effects in the first hours, while 45 mg/kg of tramadol promoted sleep first, but induced wakefulness thereafter. During non-REM sleep, tramadol (15 and 45 mg/kg) increased delta and decreased alpha power, while all doses increased gamma power. In conclusion, the sleep-related and qEEG effects of tramadol suggest antidepressant-like properties, including specific beneficial effects in selected patient groups, and raise the possibility of a faster acting antidepressant action.

Examining Sex Differences in Response to NMDAR Antagonist MK‐801 on Sleep Architecture and Brain Function Using Electroencephalography in Rats

Accumulating evidence suggests glutamatergic hypofunction is one underlying factor in the pathology of schizophrenia. Administration of N-methyl-D-aspartate receptor (NMDAR) antagonists induces psychotomimetic-like symptoms in healthy humans and has emerged as a pharmacological model for symptoms of schizophrenia in animals. MK-801, an NMDAR antagonist, is frequently used to disrupt cognition and induce hyperlocomotion, modelling the cognitive and positive symptoms of schizophrenia, respectively. However, despite significant contributions of these models to surrounding literature, there are vast sex differences in the symptomology of schizophrenia in the human population that are underrepresented in animal models. Evidence suggests that prevalence and severity of negative and cognitive symptoms may be greater in males relative to females. Furthermore, sleep disturbances are underappreciated symptoms of schizophrenia, and sex differences in these have also been reported. Applying a translational biomarker approach that can be readily implemented in human subjects, present studies used polysomnography and quantitative electroencephalography (qEEG) measures to determine if NMDAR antagonists can reveal sex differences on sleep and brain function in animals similar to those reported in the human population. EEG surface electrodes and wireless transmitters were implanted in male and female Sprague-Dawley rats. EEG's were recorded for 24 hours in freely moving rats from their homecage. MK-801 (males: 0.056-0.56 mg/kg, sc; females: 0.03-0.3 mg/kg, sc) was administered 2 hours into the light cycle. Recordings were manually scored into wake, rapid eye movement (REM), and non-REM sleep, and qEEG spectral power was evaluated during waking epochs only. Activity counts were also simultaneously recorded. Consistent with previous literature, MK-801 induced hyperlocomotion, increased time awake, and decreased both NREM and REM sleep. Females were more sensitive than males to all of these measures, showing longer duration and magnitude of effects. Furthermore, MK-801 induced profound dose-dependent increases on both low and high gamma power in male rats. Interestingly, no comparable dose-dependent increases in gamma power were found in female rats across a full log unit dose range. Gamma power is highly sensitive to glutamate function, and abnormalities have been associated with cognitive impairment and psychotic symptoms in patients with schizophrenia. This is the first report, to our knowledge, of a blunted response to MK-801's effects in female rats compared to males despite increased sensitivity to all other reported measures. Ultimately, EEG revealed sex-related differences in NMDAR function which may correspond with prevalence/severity of symptoms of schizophrenia in humans. This may overall strengthen the validity of using NMDAR antagonism in preclinical model to experimentally induce schizophrenia-like symptoms.

Cognitive Effects of Montelukast: A Pharmaco-EEG Study.

Montelukast is a well-established antiasthmatic drug with little side effects. It is a leukotriene receptor antagonist and recent research suggests cognitive benefits from its anti-inflammatory actions on the central nervous system. However, changes in brain activity were not directly shown so far in humans. This study aims to document changes in brain activity that are associated with cognitive improvement during treatment with Montelukast. We recorded EEG and conducted neuropsychological tests in 12 asthma-patients aged 38–73 years before and after 8 weeks of treatment with Montelukast. We found no significant changes on neuropsychological scales for memory, attention, and mood. In the EEG, we found decreased entropy at follow up during rest (p < 0.005). During episodic memory acquisition we found decreased entropy (p < 0.01) and acceleration of the background rhythm (p < 0.05). During visual attention performance, we detected an increase in gamma power (p < 0.005) and slowing of the background rhythm (p < 0.05). The study is limited by its small sample size, young age and absence of baseline cognitive impairment of the participants. Unspecific changes in brain activity were not accompanied by cognitive improvement. Future studies should examine elderly patients with cognitive impairment in a double-blind study with longer-term treatment by Montelukast.

Effects of antipsychotic drugs and potassium channel modulators on spectral properties of local field potentials in mouse hippocampus and pre-frontal cortex

Local field potentials (LFPs) recorded intracranially display a range of location-specific oscillatory spectra which have been related to cognitive processes. Although the mechanisms producing LFPs are not completely understood, it is likely that voltage-gated ion channels which produce action potentials and patterned discharges play a significant role. It is also known that antipsychotic drugs (APDs) affect LFP spectra and a direct inhibitory effect on voltage-gated potassium channels has been reported. Additionally, voltage-gated potassium channels have been implicated in the pathophysiology of schizophrenia, a disorder for which APDs are primary therapies. In this study we sought to: i) better characterise the effects of two APDs on LFPs spectra and connectivity measures and ii) examine the effects of potassium channel modulators on LFPs and potential overlap of effects with APDs. Intracranial electrodes were implanted in hippocampus (HIP) and pre-frontal cortex (PFC) of C57BL/6J mice; power spectra, coherence and phase-amplitude cross-frequency coupling were measured. Drugs tested were APDs haloperidol and clozapine as well as voltage-gated potassium channel modulators (KVMs) 4-aminopyridine (4-AP), tetraethylammonium, retigabine and E−4031. Both APDs and KVMs significantly reduced gamma power except 4-AP, which conversely increased gamma power. Clozapine and retigabine additionally reduced gamma coherence between HIP and PFC, while 4-AP demonstrated the opposite effect. Phase-amplitude coupling between theta and gamma oscillations in HIP was significantly reduced by the administration of haloperidol and retigabine. These results provide previously undescribed effects of APDs on LFP properties and demonstrate novel modulation of LFP characteristics by KVMs that intriguingly overlap with the APD effects.

Neural Correlates of the Shamanic State of Consciousness.

Psychedelics have been recognized as model interventions for studying altered states of consciousness. However, few empirical studies of the shamanic state of consciousness, which is anecdotally similar to the psychedelic state, exist. We investigated the neural correlates of shamanic trance using high-density electroencephalography (EEG) in 24 shamanic practitioners and 24 healthy controls during rest, shamanic drumming, and classical music listening, followed by an assessment of altered states of consciousness. EEG data were used to assess changes in absolute power, connectivity, signal diversity, and criticality, which were correlated with assessment measures. We also compared assessment scores to those of individuals in a previous study under the influence of psychedelics. Shamanic practitioners were significantly different from controls in several domains of altered states of consciousness, with scores comparable to or exceeding that of healthy volunteers under the influence of psychedelics. Practitioners also displayed increased gamma power during drumming that positively correlated with elementary visual alterations. Furthermore, shamanic practitioners had decreased low alpha and increased low beta connectivity during drumming and classical music and decreased neural signal diversity in the gamma band during drumming that inversely correlated with insightfulness. Finally, criticality in practitioners was increased during drumming in the low and high beta and gamma bands, with increases in the low beta band correlating with complex imagery and elementary visual alterations. These findings suggest that psychedelic drug-induced and non-pharmacologic alterations in consciousness have overlapping phenomenal traits but are distinct states of consciousness, as reflected by the unique brain-related changes during shamanic trance compared to previous literature investigating the psychedelic state.

EEG changes reflecting pain: is alpha suppression better than gamma enhancement?

ObjectiveSuppression of alpha and enhancement of gamma electroencephalographic (EEG) power have both been suggested as objective indicators of cortical pain processing. While gamma activity has been emphasized as the best potential marker, its spectral overlap with pain-related muscular responses is a potential drawback. Since muscle contractions are almost universal concomitants of physical pain, here we investigated alpha and gamma scalp-recorded activities during either tonic pain or voluntary facial grimaces mimicking those triggered by pain. MethodsHigh-density EEG (128 electrodes) was recorded while 14 healthy participants either underwent a cold pressor test (painful hand immersion in 10 °C water) or produced stereotyped facial/nuchal contractions (grimaces) mimicking those evoked by pain. The scalp distribution of spectral EEG changes was quantified via vector-transformation of maps and compared between the pain and grimacing conditions by calculating the cosine of the angle between the two corresponding topographies. ResultsPainful stimuli significantly enhanced gamma power bilaterally in fronto-temporal regions and decreased alpha power in the contralateral central scalp. Sustained cervico-facial contractions (grimaces) gave also rise to significant gamma power increase in fronto-temporal regions but did not decrease central scalp alpha. While changes in alpha topography significantly differed between the pain and grimace situations, the scalp topography of gamma power was statistically indistinguishable from that occurring during grimaces. ConclusionGamma power induced by painful stimuli or voluntary facial-cervical muscle contractions had overlapping topography. Pain-related alpha decrease in contralateral central scalp was less disturbed by muscle activity and may therefore prove more discriminant as an ancillary pain biomarker.

Increased aperiodic gamma power in young boys with Fragile X Syndrome is associated with better language ability

BackgroundThe lack of robust and reliable clinical biomarkers in Fragile X Syndrome (FXS), the most common inherited form of intellectual disability, has limited the successful translation of bench-to-bedside therapeutics. While numerous drugs have shown promise in reversing synaptic and behavioral phenotypes in mouse models of FXS, none have demonstrated clinical efficacy in humans. Electroencephalographic (EEG) measures have been identified as candidate biomarkers as EEG recordings of both adults with FXS and mouse models of FXS consistently exhibit alterations in resting state and task-related activity. However, the developmental timing of these EEG differences is not known as thus far EEG studies have not focused on young children with FXS. Further, understanding how EEG differences are associated with core symptoms of FXS is crucial to successful use of EEG as a biomarker, and may improve our understanding of the disorder.MethodsResting-state EEG was collected from FXS boys with full mutation of Fmr1 (2.5–7 years old, n = 11) and compared with both age-matched (n = 12) and cognitive-matched (n = 12) typically developing boys. Power spectra (including aperiodic and periodic components) were compared using non-parametric cluster-based permutation testing. Associations between 30 and 50 Hz gamma power and cognitive, language, and behavioral measures were evaluated using Pearson correlation and linear regression with age as a covariate.ResultsFXS participants showed increased power in the beta/gamma range (~ 25–50 Hz) across multiple brain regions. Both a reduction in the aperiodic (1/f) slope and increase in beta/gamma periodic activity contributed to the significant increase in high-frequency power. Increased gamma power, driven by the aperiodic component, was associated with better language ability in the FXS group. No association was observed between gamma power and parent report measures of behavioral challenges, sensory hypersensitivities, or adaptive behaviors.LimitationsThe study sample size was small, although comparable to other human studies in rare-genetic disorders. Findings are also limited to males in the age range studied.ConclusionsResting-state EEG measures from this study in young boys with FXS identified similar increases in gamma power previously reported in adults and mouse models. The observed positive association between resting state aperiodic gamma power and language development supports hypotheses that alterations in some EEG measures may reflect ongoing compensatory mechanisms.

Blink- and saccade-related suppression effects in early visual areas of the human brain: Intracranial EEG investigations during natural viewing conditions

Blinks and saccades, both ubiquitous in natural viewing conditions, cause rapid changes of visual inputs that are hardly consciously perceived. The neural dynamics in early visual areas of the human brain underlying this remarkable visual stability are still incompletely understood. We used electrocorticography (ECoG) from electrodes directly implanted on the human early visual areas V1, V2, V3d/v, V4d/v and the fusiform gyrus to investigate blink- and saccade-related neuronal suppression effects during non-experimental, free viewing conditions. We found a characteristic, biphasic, broadband gamma power decrease-increase pattern in all investigated visual areas. During saccades, a decrease in gamma power clearly preceded eye movement onset, at least in V1. This may indicate that cortical information processing is actively suppressed in human early visual areas before and during saccades, which then possibly mediates perceptual visual suppression. The following eye movement offset-related increase in gamma power may indicate the recovery of visual perception and the resumption of visual processing.

The Consciousness State of Traditional Nidrâ Yoga/Modern Yoga Nidra: Phenomenological Characterization and Preliminary Insights from an EEG Study.

Nidrâ yoga is an ancient yogic practice capable of inducing altered states of consciousness characterized by deep relaxation, strong concentration, acute self-awareness, and joy. In modern contemplative neuroscience language, it is known by the name yoga nidra, and few studies have investigated its phenomenological and psychophysiological effects. Six healthy volunteers (four females aged 31-74) performed 12 yoga nidra sessions guided by an expert during a 6-day retreat. Each session consisted of 10 minutes in a resting state (baseline) followed by 2 hours of yoga nidra. Psychometric data regarding dissociative experiences (Clinician Administered Dissociative States Scale) and the state of consciousness (Phenomenology of Consciousness Inventory) were collected after baseline and yoga nidra, while high-density EEG was recorded during the entire session. During nidra sessions, no sleep hallmarks (i.e., K-complexes and sleep spindles) were detected by the EEG in any subject. Psychometric data we re analyzed using a Wilcoxon signed-rank test corrected with the false discovery rate approach for multiple comparisons. Compared to baseline, yoga nidra practice was related to: (1) increased dissociative effects (p = 0.022); (2) perception of being in an altered state of consciousness (p = 0.026); (3) alterations in perceived body image (p = 0.022); (4) increased "meaningfulness" attributed to the experience (p = 0.026); (5) reduced rational thinking (p = 0.029); and (6) reduced volitional thought control (p = 0.026). First-person experience is discussed in relation to descriptive EEG power spectral density analysis, which was performed in one subject because of severe EEG artifacts in the other recordings; that subject showed, compared to baseline: (1) early increase of alpha and beta power, followed by a progressive widespread reduction; (2) widespread early increase of theta power, followed by a progressive reduction; and (3) widespread increase of gamma power in the latest stages. The present preliminary results enrich the knowledge of yoga nidra, elucidating its phenomenology and suggesting some psychophysiological correlates that future studies may address.

Gamma power increased in Alzheimer's disease patients in comparison to healthy controls during recognition of facial expressions

AbstractBackgroundSeveral researchers have reported the impairment of recognition of facial expressions in Alzheimer’s disease (AD) patients. AD had reduced theta and alpha responses compared to healthy controls during the recognition of facial expressions (Güntekin et al. 2019). Gamma responses also have a crucial role in the recognition of facial expression in healthy young adults (Güntekin and Başar 2014). AD had increased late gamma responses compared to healthy controls during working memory paradigms (Başar et al. 2017). The present study aims to analyze the gamma responses during the recognition of facial expressions in AD and healthy controls. We hypothesized that if the increase of late gamma responses is a general phenomenon in AD patients independent of the stimulation type, we expect to find increase gamma responses in AD patients in comparison to healthy controls.MethodEEGs of 40 healthy controls (HCs) and 41 AD patients were recorded during their perception of three different facial expressions (angry, happy, neutral). Event‐related power spectrum and phase locking were analyzed for three different gamma bands (30‐35 Hz, 35‐ 40Hz, 40‐48 Hz) in two different time windows (0‐200 ms, 200‐400 ms).ResultThe group difference between AD patients and HCs was not significant for the phase‐locking values. AD patients had higher gamma power responses compared to healthy controls in 200‐400 ms time window for 30‐35 Hz(p=0.016), 35‐40 Hz(p=0.018) and 40‐48 Hz (p=0.039). The only significant group difference for the early time window (0‐200 ms) was found for 35‐40 Hz (p=0.046). The figure shows topographical plots of gamma (35‐40 Hz) power for 200‐400 ms time window in patients (upper part) and healthy controls (lower part) for angry, happy and neutral facial expressions.ConclusionThe present study showed that the increase of late (200‐400 ms) gamma were independent of stimulus type in AD patients. The increase of gamma power in a 200‐400 ms time window was found in AD patients compared to healthy controls for all three facial expressions. The facial expression recognition in AD patients was differentiated from healthy controls by increased gamma power. Acknowledgments: This work (grant number 218S314) was supported by TUBITAK.

Cross-frequency coupling between gamma oscillations and deep brain stimulation frequency in Parkinson's disease.

The disruption of pathologically enhanced beta oscillations is considered one of the key mechanisms mediating the clinical effects of deep brain stimulation on motor symptoms in Parkinson's disease. However, a specific modulation of other distinct physiological or pathological oscillatory activities could also play an important role in symptom control and motor function recovery during deep brain stimulation. Finely tuned gamma oscillations have been suggested to be prokinetic in nature, facilitating the preferential processing of physiological neural activity. In this study, we postulate that clinically effective high-frequency stimulation of the subthalamic nucleus imposes cross-frequency interactions with gamma oscillations in a cortico-subcortical network of interconnected regions and normalizes the balance between beta and gamma oscillations. To this end we acquired resting state high-density (256 channels) EEG from 31 patients with Parkinson's disease who underwent deep brain stimulation to compare spectral power and power-to-power cross-frequency coupling using a beamformer algorithm for coherent sources. To show that modulations exclusively relate to stimulation frequencies that alleviate motor symptoms, two clinically ineffective frequencies were tested as control conditions. We observed a robust reduction of beta and increase of gamma power, attested in the regions of a cortical (motor cortex, supplementary motor area, premotor cortex) and subcortical network (subthalamic nucleus and cerebellum). Additionally, we found a clear cross-frequency coupling of narrowband gamma frequencies to the stimulation frequency in all of these nodes, which negatively correlated with motor impairment. No such dynamics were revealed within the control posterior parietal cortex region. Furthermore, deep brain stimulation at clinically ineffective frequencies did not alter the source power spectra or cross-frequency coupling in any region. These findings demonstrate that clinically effective deep brain stimulation of the subthalamic nucleus differentially modifies different oscillatory activities in a widespread network of cortical and subcortical regions. Particularly the cross-frequency interactions between finely tuned gamma oscillations and the stimulation frequency may suggest an entrainment mechanism that could promote dynamic neural processing underlying motor symptom alleviation.

Large effects of brief meditation intervention on EEG spectra in meditation novices

This study investigated the impact of a brief meditation workshop on a sample of 223 novice meditators. Participants attended a three-day workshop comprising daily guided seated meditation sessions using music without vocals that focused on various emotional states and intentions (open focus). Based on the theory of integrative consciousness, it was hypothesized that altered states of consciousness would be experienced by participants during the meditation intervention as assessed using electroencephalogram (EEG). Brainwave power bands patterns were measured throughout the meditation training workshop, producing a total of 5616 EEG scans. Changes in conscious states were analysed using pre-meditation and post-meditation session measures of delta through to gamma oscillations. Results suggested the meditation intervention had large varying effects on EEG spectra (up to 50 % increase and 24 % decrease), and the speed of change from pre-meditation to post-meditation state of the EEG co-spectra was significant (with 0.76 probability of entering end-meditation state within the first minute). There was a main 5 % decrease in delta power (95 % HDI = [−0.07, −0.03]); a global increase in theta power of 29 % (95 % HDI = [0.27, 0.33]); a global increase of 16 % (95 % HDI = [0.13, 0.19]) in alpha power; a main effect of condition, with global beta power increasing by 17 % (95 % HDI = [0.15, 0.19]); and an 11 % increase (95 % HDI = [0.08, 0.14]) in gamma power from pre-meditation to end-meditation. Findings provided preliminary support for brief meditation in altering states of consciousness in novice meditators. Future clinical examination of meditation was recommended as an intervention for mental health conditions particularly associated with hippocampal impairments.

Age- and movement-related modulation of cortical oscillations in a mouse model of presbycusis

Brain oscillations are associated with specific cognitive and sensory processes. How age-related hearing loss (presbycusis) alters cortical oscillations is unclear. Altered inhibitory neurotransmission and temporal processing deficits contribute to speech recognition impairments in presbycusis. Specifically, age-related reduction in parvalbumin positive interneurons and perineuronal nets in the auditory cortex predicts a reduction in gamma oscillations that may lead to a decline in temporal precision and attention. To test the hypothesis that resting and evoked gamma oscillations decline with presbycusis, EEGs were recorded from the auditory and frontal cortex of awake, freely moving C57BL/6 J mice at three ages (3, 14 and 24 months). Resting EEG data were analyzed according to movement state (move versus still). Evoked responses were recorded following presentation of noise bursts or amplitude modulated noise with time varying modulation frequencies. We report an age-related decrease in resting gamma power, a decline in gamma-range synchrony to time varying stimuli, and an increase in noise evoked and induced gamma power. A decline in temporal processing is seen in aged mice that exhibit robust auditory-evoked potentials, dissociating hearing loss from temporal processing deficits. We also report an increase in gamma power when mice moved compared to the still state. However, the movement-related modulation of gamma oscillations did not change with age. Together, these data identify a number of novel markers of presbycusis-related changes in auditory and frontal cortex. Because EEGs are commonly recorded in humans, the mouse data may serve as translation relevant preclinical biomarkers to facilitate the development of therapeutics to delay or reverse central auditory processing deficits in presbycusis.