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Changes in brain oscillatory activity are commonly used as biomarkers both in cognitive neuroscience and in neuropsychiatric conditions. However, little is known about how its profile changes across maturation. Here we use regression models to characterize magnetoencephalography power changes within classical frequency bands in a sample of 792 healthy participants, covering the range 13 to 80 years old. Our findings unveil complex, non-linear power trajectories that defy the traditional linear paradigm, with notable cortical region variations. Interestingly, slow wave activity increases correlate with improved cognitive performance throughout life and larger gray matter volume in the elderly. Conversely, fast wave activity diminishes in adulthood. Elevated low-frequency activity during aging, traditionally seen as compensatory, may also signify neural deterioration. This dual interpretation, highlighted by our study, reveals the intricate dynamics between brain oscillations, cognitive performance, and aging. It advances our understanding of neurodevelopment and aging by emphasizing the regional specificity and complexity of brain rhythm changes, with implications for cognitive and structural integrity. Key points: • Non-Linear brain activity trajectories: The study challenges linear brain activity changes with age, revealing distinct trajectories in oscillatory patterns based on frequency and brain region. • Contradicting age-related slowing: slow wave activity decreases and fast wave activity increases during healthy aging, contrasting with pathological conditions. • Cognitive implications and structural integrity: Oscillatory power changes correlate with cognitive decline and reduced structural integrity, challenging the brain scaffolding theory of aging and offering insights into neurodevelopment and aging. [ABSTRACT FROM AUTHOR]

Traditionally, pitch variation in a sound stream has been integral to music identity. We attempt to expand music's definition, by demonstrating that the neural code for musicality is independent of pitch encoding. That is, pitchless sound streams can still induce music-like perception and a neurophysiological hierarchy similar to pitched melodies. Previous work reported that neural processing of sounds with no-pitch, fixed-pitch, and irregular-pitch (melodic) patterns, exhibits a right-lateralized hierarchical shift, with pitchless sounds favorably processed in Heschl's gyrus (HG), ascending laterally to nonprimary auditory areas for fixed-pitch and even more laterally for melodic patterns. The objective of this EEG study was to assess whether sound encoding maintains a similar hierarchical profile when musical perception is driven by timbre irregularities in the absence of pitch changes. Individuals listened to repetitions of three musical and three nonmusical sound-streams. The nonmusical streams were comprised of seven 200-ms segments of white, pink, or brown noise, separated by silent gaps. Musical streams were created similarly, but with all three noise types combined in a unique order within each stream to induce timbre variations and music-like perception. Subjects classified the sound streams as musical or nonmusical. Musical processing exhibited right dominant α power enhancement, followed by a lateralized increase in θ phase-locking and spectral power. The θ phase-locking was stronger in musicians than in nonmusicians. The lateralization of activity suggests higher-level auditory processing. Our findings validate the existence of a hierarchical shift, traditionally observed with pitched-melodic perception, underscoring that musicality can be achieved with timbre irregularities alone.NEW & NOTEWORTHY EEG induced by streams of pitchless noise segments varying in timbre were classified as music-like and exhibited a right-lateralized hierarchy in processing similar to pitched melodic processing. This study provides evidence that the neural-code of musicality is independent of pitch encoding. The results have implications for understanding music processing in individuals with degraded pitch perception, such as in cochlear-implant listeners, as well as the role of nonpitched sounds in the induction of music-like perceptual states.

Background: Cognitive deficits observed in Alzheimer's disease (AD) patients have been correlated with altered hippocampal activity. Although the mechanism remains under extensive study, neurofibrillary tangles and amyloid plaques have been proposed as responsible for brain activity alterations. Aiming to unveil the mechanism, researchers have developed several transgenic models of AD. Nevertheless, the variability in hippocampal oscillatory alterations found in different genetic backgrounds and ages remains unclear. Objective: To assess the oscillatory alterations in relation to animal developmental age and protein inclusion, amyloid-β (Aβ) load, and abnormally phosphorylated tau (pTau), we reviewed and analyzed the published data on peak power, frequency, and quantification of theta-gamma cross-frequency coupling (modulation index values). Methods: To ensure that the search was as current as possible, a systematic review was conducted to locate and abstract all studies published from January 2000 to February 2023 that involved in vivo hippocampal local field potential recording in transgenic mouse models of AD. Results: The presence of Aβ was associated with electrophysiological alterations that are mainly reflected in power increases, frequency decreases, and lower modulation index values. Concomitantly, pTau accumulation was associated with electrophysiological alterations that are mainly reflected in power decreases, frequency decreases, and no significant alterations in modulation index values. Conclusions: In this study, we showed that electrophysiological parameters are altered from prodromal stages to the late stages of pathology. Thus, we found that Aβ deposition is associated with brain network hyperexcitability, whereas pTau deposition mainly leads to brain network hypoexcitability in transgenic models [ABSTRACT FROM AUTHOR]

Paroxysmal kinesigenic dyskinesia (PKD) is associated with a disturbance of neural circuit and network activities, while its neurophysiological characteristics have not been fully elucidated. This study utilized the high‐density electroencephalogram (hd‐EEG) signals to detect abnormal brain activity of PKD and provide a neural biomarker for its clinical diagnosis and PKD progression monitoring. The resting hd‐EEGs are recorded from two independent datasets and then source‐localized for measuring the oscillatory activities and function connectivity (FC) patterns of cortical and subcortical regions. The abnormal elevation of theta oscillation in wildly brain regions represents the most remarkable physiological feature for PKD and these changes returned to healthy control level in remission patients. Another remarkable feature of PKD is the decreased high‐gamma FCs in non‐remission patients. Subtype analyses report that increased theta oscillations may be related to the emotional factors of PKD, while the decreased high‐gamma FCs are related to the motor symptoms. Finally, the authors established connectome‐based predictive modelling and successfully identified the remission state in PKD patients in dataset 1 and dataset 2. The findings establish a clinically relevant electroencephalography profile of PKD and indicate that hd‐EEG can provide robust neural biomarkers to evaluate the prognosis of PKD. [ABSTRACT FROM AUTHOR]

Abstract Paroxysmal kinesigenic dyskinesia (PKD) is associated with a disturbance of neural circuit and network activities, while its neurophysiological characteristics have not been fully elucidated. This study utilized the high‐density electroencephalogram (hd‐EEG) signals to detect abnormal brain activity of PKD and provide a neural biomarker for its clinical diagnosis and PKD progression monitoring. The resting hd‐EEGs are recorded from two independent datasets and then source‐localized for measuring the oscillatory activities and function connectivity (FC) patterns of cortical and subcortical regions. The abnormal elevation of theta oscillation in wildly brain regions represents the most remarkable physiological feature for PKD and these changes returned to healthy control level in remission patients. Another remarkable feature of PKD is the decreased high‐gamma FCs in non‐remission patients. Subtype analyses report that increased theta oscillations may be related to the emotional factors of PKD, while the decreased high‐gamma FCs are related to the motor symptoms. Finally, the authors established connectome‐based predictive modelling and successfully identified the remission state in PKD patients in dataset 1 and dataset 2. The findings establish a clinically relevant electroencephalography profile of PKD and indicate that hd‐EEG can provide robust neural biomarkers to evaluate the prognosis of PKD.

In today's digital information age, human exposure to visual artifacts has reached an unprecedented quasi-omnipresence. Some of these cultural artifacts are elevated to the status of artworks which indicates a special appreciation of these objects. For many persons, the perception of such artworks coincides with aesthetic experiences (AE) that can positively affect health and wellbeing. AEs are composed of complex cognitive and affective mental and physiological states. More profound scientific understanding of the neural dynamics behind AEs would allow the development of passive Brain-Computer-Interfaces (BCI) that offer personalized art presentation to improve AE without the necessity of explicit user feedback. However, previous empirical research in visual neuroaesthetics predominantly investigated functional Magnetic Resonance Imaging and Event-Related-Potentials correlates of AE in unnaturalistic laboratory conditions which might not be the best features for practical neuroaesthetic BCIs. Furthermore, AE has, until recently, largely been framed as the experience of beauty or pleasantness. Yet, these concepts do not encompass all types of AE. Thus, the scope of these concepts is too narrow to allow personalized and optimal art experience across individuals and cultures. This narrative mini-review summarizes the state-of-the-art in oscillatory Electroencephalography (EEG) based visual neuroaesthetics and paints a road map toward the development of ecologically valid neuroaesthetic passive BCI systems that could optimize AEs, as well as their beneficial consequences. We detail reported oscillatory EEG correlates of AEs, as well as machine learning approaches to classify AE. We also highlight current limitations in neuroaesthetics and suggest future directions to improve EEG decoding of AE.

Introduction: Sound therapy is a common tinnitus treatment, where the tinnitus percept is either fully or partially masked by an external sound. Some tinnitus patients experience a decrease in tinnitus related distress after the use of sound therapy. Differences in the neural response to sound therapy may form a basis for classifying tinnitus patients. Methods: In this study, the long-term (2 months) effects of sound therapy on the oscillatory brain activity and tinnitus related distress were investigated in chronic tinnitus patients. Baseline oscillatory activity in the group of tinnitus participants was also compared to a matched control group. Results: No differences were found in the oscillatory activity when comparing the tinnitus group to the control group. Differences were found for the frequency range between 27.5 and 41.5 Hz corresponding to high beta and gamma power when comparing the tinnitus group before and after the use of sound therapy. Furthermore, a reduction of the tinnitus-related distress was found after the long-term use of sound therapy. However, there was no correlation between the changes in the oscillatory activity and the reductions of the tinnitus-related distress. Discussion: Overall, the lack of correlation between the changes in tinnitusrelated distress and changes in power activity hampers the interpretability of the findings and undermines the utility of using oscillatory activity as a biomarker for the effect of sound therapy treatment. [ABSTRACT FROM AUTHOR]

Carnitine palmitoyltransferase 1c (CPT1C) is a neuron‐specific protein widely distributed throughout the CNS and highly expressed in discrete brain areas including the hypothalamus, hippocampus, amygdala and different motor regions. Its deficiency has recently been shown to disrupt dendritic spine maturation and AMPA receptor synthesis and trafficking in the hippocampus, but its contribution to synaptic plasticity and cognitive learning and memory processes remains mostly unknown. Here, we aimed to explore the molecular, synaptic, neural network and behavioural role of CPT1C in cognition‐related functions by using CPT1C knockout (KO) mice. CPT1C‐deficient mice showed extensive learning and memory deficits. The CPT1C KO animals exhibited impaired motor and instrumental learning that seemed to be related, in part, to locomotor deficits and muscle weakness but not to mood alterations. In addition, CPT1C KO mice showed detrimental hippocampus‐dependent spatial and habituation memory, most probably attributable to inefficient dendritic spine maturation, impairments in long‐term plasticity at the CA3–CA1 synapse and aberrant cortical oscillatory activity. In conclusion, our results reveal that CPT1C is not only crucial for motor function, coordination and energy homeostasis, but also has a crucial role in the maintenance of learning and memory cognitive functions. Key points: CPT1C, a neuron‐specific interactor protein involved in AMPA receptor synthesis and trafficking, was found to be highly expressed in the hippocampus, amygdala and various motor regions.CPT1C‐deficient animals exhibited energy deficits and impaired locomotion, but no mood changes were found.CPT1C deficiency disrupts hippocampal dendritic spine maturation and long‐term synaptic plasticity and reduces cortical γ oscillations.CPT1C was found to be crucial for motor, associative and non‐associative learning and memory. [ABSTRACT FROM AUTHOR]

Brain–body interactions (BBIs) have been the focus of intense scrutiny since the inception of the scientific method, playing a foundational role in the earliest debates over the philosophy of science. Contemporary investigations of BBIs to elucidate the neural principles of motor control have benefited from advances in neuroimaging, device engineering, and signal processing. However, these studies generally suffer from two major limitations. First, they rely on interpretations of 'brain' activity that are behavioral in nature, rather than neuroanatomical or biophysical. Second, they employ methodological approaches that are inconsistent with a dynamical systems approach to neuromotor control. These limitations represent a fundamental challenge to the use of BBIs for answering basic and applied research questions in neuroimaging and neurorehabilitation. Thus, this review is written as a tutorial to address both limitations for those interested in studying BBIs through a dynamical systems lens. First, we outline current best practices for acquiring, interpreting, and cleaning scalp-measured electroencephalography (EEG) acquired during whole-body movement. Second, we discuss historical and current theories for modeling EEG and kinematic data as dynamical systems. Third, we provide worked examples from both canonical model systems and from empirical EEG and kinematic data collected from two subjects during an overground walking task. [ABSTRACT FROM AUTHOR]

Background: Suboptimal performance during neuropsychological testing frequently occurs in multiple sclerosis (MS), leading to unreliable cognitive outcomes. Neurophysiological alterations correlate with MS-related cognitive impairment, but studies have not yet considered performance validity. Objectives: To investigate neurophysiological markers of cognitive impairment in MS, while explicitly addressing performance validity. Methods: Magnetoencephalography recordings, neuropsychological assessments, and performance validity testing were obtained from 90 MS outpatients with cognitive complaints. Spectral and resting-state functional connectivity (rsFC) properties were compared between cognitively impaired (CI), cognitively preserved (CP), and suboptimally performing (SUB) patients using regression models and permutation testing. Results: CI had higher power in low-frequency bands and lower power in high bands compared to CP, indicating neuronal slowing. CI also showed lower beta power compared to SUB. Overall power spectra visually differed between CI and CP, and SUB showed overlap with both groups. CI had lower rsFC than CP and SUB patients. CP and SUB patients showed no differences. Conclusion: Neuronal slowing and altered rsFC can be considered cognitive markers in MS. Patients who performed suboptimally showed resemblance with patients with and without cognitive impairments, and although their overall neurophysiological profile was more similar to patients without impairments, it suggests heterogeneity regarding their pathophysiology. [ABSTRACT FROM AUTHOR]

• Theta/gamma co-modulation correlates with the spatial working memory in mice. • NMDAr blockade by MK-801 impairs the association of oscillatory activity and performance. • NMDAr blockade by MK-801 alters the normal correlation of hippocampal rhythms and the speed of movement. • These results shed light into the oscillatory mechanisms altered in working memory in schizophrenia. Abnormal N-methyl-D-aspartate receptor (NMDAr) function has been linked to oscillopathies, psychosis, and cognitive dysfunction in schizophrenia (SCZ). Here, we investigate the role of NMDAr hypofunction in pathological oscillations and behavior. We implanted mice with tetrodes in the dorsal/intermediate hippocampus and medial prefrontal cortex (mPFC), administered the NMDAr antagonist MK-801, and recorded oscillations during spontaneous exploration in an open field and in the y-maze spatial working memory test. Our results show that NMDAr blockade disrupted the correlation between oscillations and speed of movement, crucial for internal representations of distance. In the hippocampus, MK-801 increased gamma oscillations and disrupted theta/gamma coupling during spatial working memory. In the mPFC, MK-801 increased the power of theta and gamma, generated high-frequency oscillations (HFO 155–185 Hz), and disrupted theta/gamma coupling. Moreover, the performance of mice in the spatial working memory version of the y-maze was strongly correlated with CA1-PFC theta/gamma co-modulation. Thus, theta/gamma mediated by NMDAr function might explain several of SCZ's cognitive symptoms and might be crucial to explaining hippocampal-PFC interaction. [ABSTRACT FROM AUTHOR]

IntroductionSound therapy is a common tinnitus treatment, where the tinnitus percept is either fully or partially masked by an external sound. Some tinnitus patients experience a decrease in tinnitus related distress after the use of sound therapy. Differences in the neural response to sound therapy may form a basis for classifying tinnitus patients.MethodsIn this study, the long-term (2 months) effects of sound therapy on the oscillatory brain activity and tinnitus related distress were investigated in chronic tinnitus patients. Baseline oscillatory activity in the group of tinnitus participants was also compared to a matched control group.ResultsNo differences were found in the oscillatory activity when comparing the tinnitus group to the control group. Differences were found for the frequency range between 27.5 and 41.5 Hz corresponding to high beta and gamma power when comparing the tinnitus group before and after the use of sound therapy. Furthermore, a reduction of the tinnitus-related distress was found after the long-term use of sound therapy. However, there was no correlation between the changes in the oscillatory activity and the reductions of the tinnitus-related distress.DiscussionOverall, the lack of correlation between the changes in tinnitus-related distress and changes in power activity hampers the interpretability of the findings and undermines the utility of using oscillatory activity as a biomarker for the effect of sound therapy treatment.

Oscillatory activity in the cerebellum and linked networks is an important aspect of neuronal processing and functional implementation of behavior. So far, it was challenging to quantify and study cerebellar oscillatory signatures in human neuroscience due to the constraints of non-invasive cerebellar electrophysiological recording and interventional techniques. The emerging cerebellar transcranial alternating current stimulation technique (CB-tACS) is a promising tool, which may partially overcome this challenge and provides an exciting non-invasive opportunity to better understand cerebellar physiology. Several studies have successfully demonstrated that CB-tACS can modulate the cerebellar outflow and cerebellum-linked behavior. In the present narrative review, we summarize current studies employing the CB-tACS approach and discuss open research questions. Hereby, we aim to provide an overview on this emerging electrophysiological technique and strive to promote future research in the field. CB-tACS will contribute in the further deciphering of cerebellar oscillatory signatures and its role for motor, cognitive, or affective functions. In long term, CB-tACS could develop into a therapeutic tool for retuning disturbed oscillatory activity in cerebellar networks underlying brain disorders. [ABSTRACT FROM AUTHOR]

The exploration of various neuroimaging techniques have become focal points within the field of neuroscience research. Magnetoencephalography based on optically pumped magnetometers (OPM-MEG) has shown significant potential to be the next generation of functional neuroimaging with the advantages of high signal intensity and flexible sensor arrangement. In this study, we constructed a 31-channel OPM-MEG system and performed a preliminary comparison of the temporal and spatial relationship between magnetic responses measured by OPM-MEG and blood-oxygen-level-dependent signals detected by functional magnetic resonance imaging (fMRI) during a grasping task. For OPM-MEG, the β -band (15–30 Hz) oscillatory activities can be reliably detected across multiple subjects and multiple session runs. To effectively localize the inhibitory oscillatory activities, a source power-spectrum ratio-based imaging method was proposed. This approach was compared with conventional source imaging methods, such as minimum norm-type and beamformer methods, and was applied in OPM-MEG source analysis. Subsequently, the spatial and temporal responses at the source-level between OPM-MEG and fMRI were analyzed. The effectiveness of the proposed method was confirmed through simulations compared to benchmark methods. Our demonstration revealed an average spatial separation of 10.57 ± 4.41 mm between the localization results of OPM-MEG and fMRI across four subjects. Furthermore, the fMRI-constrained OPM-MEG localization results indicated a more focused imaging extent. Taken together, the performance exhibited by OPM-MEG positions it as a potential instrument for functional surgery assessment. • The brain responses measured by OPM-MEG and fMRI were investigated and compared. • A source power-spectrum ratio-based imaging method was proposed and applied. • Simulations and experiments validated the effectiveness of the proposed method. • Fidelities across multiple subjects and runs demonstrated the performance of OPM-MEG. [ABSTRACT FROM AUTHOR]

Alpha oscillatory activity is thought to contribute to visual expectancy through the engagement of task-relevant occipital regions. In early blindness, occipital alpha oscillations are systematically reduced, suggesting that occipital alpha depends on visual experience. However, it remains possible that alpha activity could serve expectancy in non-visual modalities in blind people, especially considering that previous research has shown the recruitment of the occipital cortex for non-visual processing. To test this idea, we used electroencephalography to examine whether alpha oscillations reflected a differential recruitment of task-relevant regions between expected and unexpected conditions in two haptic tasks (texture and shape discrimination). As expected, sensor-level analyses showed that alpha suppression in parieto-occipital sites was significantly reduced in early blind individuals compared with sighted participants. The source reconstruction analysis revealed that group differences originated in the middle occipital cortex. In that region, expected trials evoked higher alpha desynchronization than unexpected trials in the early blind group only. Our results support the role of alpha rhythms in the recruitment of occipital areas in early blind participants, and for the first time we show that although posterior alpha activity is reduced in blindness, it remains sensitive to expectancy factors. Our findings therefore suggest that occipital alpha activity is involved in tactile expectancy in blind individuals, serving a similar function to visual anticipation in sighted populations but switched to the tactile modality. Altogether, our results indicate that expectancy-dependent modulation of alpha oscillatory activity does not depend on visual experience. Significance statement: Are posterior alpha oscillations and their role in expectancy and anticipation dependent on visual experience? Our results show that tactile expectancy can modulate posterior alpha activity in blind (but not sighted) individuals through the engagement of occipital regions, suggesting that in early blindness, alpha oscillations maintain their proposed role in visual anticipation but subserve tactile processing. Our findings bring a new understanding of the role that alpha oscillatory activity plays in blindness, contrasting with the view that alpha activity is task unspecific in blind populations.

Brain–body interactions (BBIs) have been the focus of intense scrutiny since the inception of the scientific method, playing a foundational role in the earliest debates over the philosophy of science. Contemporary investigations of BBIs to elucidate the neural principles of motor control have benefited from advances in neuroimaging, device engineering, and signal processing. However, these studies generally suffer from two major limitations. First, they rely on interpretations of ‘brain’ activity that are behavioral in nature, rather than neuroanatomical or biophysical. Second, they employ methodological approaches that are inconsistent with a dynamical systems approach to neuromotor control. These limitations represent a fundamental challenge to the use of BBIs for answering basic and applied research questions in neuroimaging and neurorehabilitation. Thus, this review is written as a tutorial to address both limitations for those interested in studying BBIs through a dynamical systems lens. First, we outline current best practices for acquiring, interpreting, and cleaning scalp-measured electroencephalography (EEG) acquired during whole-body movement. Second, we discuss historical and current theories for modeling EEG and kinematic data as dynamical systems. Third, we provide worked examples from both canonical model systems and from empirical EEG and kinematic data collected from two subjects during an overground walking task.

Chronic stress contributes to the onset and exacerbation of major depressive disorder (MDD) through the oscillatory activity in the prefrontal cortex (PFC). However, the oscillations on which chronic social stress converges to yield the behavioral state of social avoidance are largely unknown. Here, we use a chronic social defeat stress model and in vivo electrophysiological recordings to uncover a novel neurophysiological measure that predicts the social behavioral state in stressed animals. First, in this study, we find that chronic social defeat stress model induces depression-like behaviors (anhedonia and social avoidance). Second, we find statistically significant differences in PFC oscillatory activity across different frequency ranges in social behavioral state, and the oscillatory activity correlates with stress-induced behavioral state. Finally, we show that the social behavioral states are accurately decoded from the oscillatory activity based on machine learning. Together, these results demonstrate that naturally occurring differences in PFC oscillation underlie the social behavioral state that accompanies the emergence of stress-induced behavioral dysfunction. [ABSTRACT FROM AUTHOR]

Exaggerated subthalamic beta oscillatory activity and increased beta range cortico-subthalamic synchrony have crystallized as the electrophysiological hallmarks of Parkinson's disease. Beta oscillatory activity is not tonic but occurs in ‘bursts’ of transient amplitude increases. In Parkinson's disease, the characteristics of these bursts are altered especially in the basal ganglia. However, beta oscillatory dynamics at the cortical level and how they compare with healthy brain activity is less well studied. We used magnetoencephalography (MEG) to study sensorimotor cortical beta bursting and its modulation by subthalamic deep brain stimulation in Parkinson's disease patients and age-matched healthy controls. We show that the changes in beta bursting amplitude and duration typical of Parkinson's disease can also be observed in the sensorimotor cortex, and that they are modulated by chronic subthalamic deep brain stimulation, which, in turn, is reflected in improved motor function at the behavioural level. In addition to the changes in individual beta bursts, their timing relative to each other was altered in patients compared to controls: bursts were more clustered in untreated Parkinson's disease, occurring in ‘bursts of bursts’, and re-burst probability was higher for longer compared to shorter bursts. During active deep brain stimulation, the beta bursting in patients resembled healthy controls’ data. In summary, both individual bursts’ characteristics and burst patterning are affected in Parkinson's disease, and subthalamic deep brain stimulation normalizes some of these changes to resemble healthy controls’ beta bursting activity, suggesting a non-invasive biomarker for patient and treatment follow-up.

A few studies have indicated that males and females respond differently to whole-body vibration (WBV) training. However, the existing insights are still insufficient and they cannot be transferred to sex-specific practice planning. To evaluate the effect of 5-week WBV training on neuromuscular [countermovement jump (CMJ), squat jump (SJ)] and cardiovascular [heart rate and blood pressure] data, taking into account sex-specific effects. This is a comparative experimental study including 96 healthy adults, divided into two groups: a WBV group (25 females and 24 males) and a control group (27 females and 20 males). The participants attended nine to ten training sessions (twice a week for 5 weeks), each lasting approximately 30 min. Both groups performed the same exercise routine on the vibration training device. For the WBV group, the training device was vibrating during the whole training session, including the breaks. For the control group, it was turned off. Maximum jump height (H, cm) and maximum relative power (MRP, kW/kg) were noted during CMJ and SJ performed on a force plate. Resting (sitting) heart rate (bpm) and blood pressure (mmHg) were measured twice, before and after the intervention. For each parameter, ∆data (= before – after) was calculated. Interactive effects of sex (2) vs group (2) vs session (2) were noted only in males and they only concerned ∆SJMPR and ∆CMJH: compared to the control group, the WBV group had better ∆SJMPR (1.39 ± 3.05 vs -2.69 ± 4.49 kW/kg, respectively) and ∆CMJH (0.50 ± 6.14 vs -4.42 ± 5.80 cm, respectively). No sex-specific effect of WBV on neuromuscular (CMJ and SJ) or cardiovascular (heart rate and blood pressure) data was found.

Background: Tau hyperphosphorylation at several sites, including those close to its microtubule domain (MD), is considered a key pathogenic event in the development of tauopathies. Nevertheless, we recently demonstrated that at the very early disease stage, tau phosphorylation (pTau) at MD sites promotes neuroprotection by preventing seizure-like activity.Objective: To further support the notion that very early pTau is not detrimental, the present work evaluated the young rTg4510 mouse model of tauopathy as a case study. Thus, in mice at one month of age (PN30-35), we studied the increase of pTau within the hippocampal area as well as hippocampal and locomotor function.Methods: We used immunohistochemistry, T-maze, nesting test, novel object recognition test, open field arena, and electrophysiology.Results: Our results showed that the very young rTg4510 mouse model has no detectable changes in hippocampal dependent tasks, such as spontaneous alternation and nesting, or in locomotor activity. However, at this very early stage the hippocampal neurons from PN30-35 rTg4510 mice accumulate pTau protein and exhibit changes in hippocampal oscillatory activity. Moreover, we found a significant reduction in the somatic area of pTau positive pyramidal and granule neurons in the young rTg4510 mice. Despite this, improved memory and increased number of dendrites per cell in granule neurons was found.Conclusion: Altogether, this study provides new insights into the early pathogenesis of tauopathies and provides further evidence that pTau remodels hippocampal function and morphology. [ABSTRACT FROM AUTHOR]

Chronic tinnitus, the continuous perception of a phantom sound, is a highly prevalent audiological symptom, for which the underlying pathology has not yet been fully understood. It is associated with neurophysiological alterations in the central nervous system and chronic stress, which can be related with a disinhibition of the inflammatory system. We here investigated the association between resting-state oscillatory activity assessed with Magnetoencephalography (MEG), and peripheral inflammation assessed by C-reactive protein (CRP) in a group of patients with chronic tinnitus (N = 21, nine males, mean age: 40.6 ± 14.6 years). Additionally, CRP was assessed in an age- and sex-matched healthy control group (N = 21, nine males, mean age: 40.9 ± 15.2 years). No MEG data was available for the control group. We found a significant negative correlation between CRP and gamma power in the orbitofrontal cortex in tinnitus patients (p < 0.001), pointing to a deactivation of the orbitofrontal cortex when CRP was high. No significant clusters were found for other frequency bands. Moreover, CRP levels were significantly higher in the tinnitus group than in the healthy controls (p = 0.045). Our results can be interpreted based on findings from previous studies having disclosed the orbitofrontal cortex as part of the tinnitus distress network. We suggest that higher CRP levels and the associated deactivation of the orbitofrontal cortex in chronic tinnitus patients is maintaining the tinnitus percept through disinhibition of the auditory cortex and attentional or emotional top-down processes. Although the direction of the association (i.e., causation) between CRP levels and orbitofrontal gamma power in chronic tinnitus is not yet known, inflammation reducing interventions are promising candidates when developing treatments for tinnitus patients. Overall, our study highlights the importance of considering immune-brain communication in tinnitus research. [ABSTRACT FROM AUTHOR]

Chronic tinnitus, the continuous perception of a phantom sound, is a highly prevalent audiological symptom, for which the underlying pathology has not yet been fully understood. It is associated with neurophysiological alterations in the central nervous system and chronic stress, which can be related with a disinhibition of the inflammatory system. We here investigated the association between resting-state oscillatory activity assessed with Magnetoencephalography (MEG), and peripheral inflammation assessed by C-reactive protein (CRP) in a group of patients with chronic tinnitus (N = 21, nine males, mean age: 40.6 ± 14.6 years). Additionally, CRP was assessed in an age- and sex-matched healthy control group (N = 21, nine males, mean age: 40.9 ± 15.2 years). No MEG data was available for the control group. We found a significant negative correlation between CRP and gamma power in the orbitofrontal cortex in tinnitus patients (p < 0.001), pointing to a deactivation of the orbitofrontal cortex when CRP was high. No significant clusters were found for other frequency bands. Moreover, CRP levels were significantly higher in the tinnitus group than in the healthy controls (p = 0.045). Our results can be interpreted based on findings from previous studies having disclosed the orbitofrontal cortex as part of the tinnitus distress network. We suggest that higher CRP levels and the associated deactivation of the orbitofrontal cortex in chronic tinnitus patients is maintaining the tinnitus percept through disinhibition of the auditory cortex and attentional or emotional top-down processes. Although the direction of the association (i.e., causation) between CRP levels and orbitofrontal gamma power in chronic tinnitus is not yet known, inflammation reducing interventions are promising candidates when developing treatments for tinnitus patients. Overall, our study highlights the importance of considering immune-brain communication in tinnitus research.

LIS1 (PAFAH1B1) plays a major role in the developing cerebral cortex, and haploinsufficient mutations cause human lissencephaly type 1. We have studied morphological and functional properties of the cerebral cortex of mutant mice harboring a deletion in the first exon of the mouse Lis1 (Pafah1b1) gene, which encodes for the LisH domain. The Lis1/sLis1 animals had an overall unaltered cortical structure but showed an abnormal distribution of cortical GABAergic interneurons (those expressing calbindin, calretinin, or parvalbumin), which mainly accumulated in the deep neocortical layers. Interestingly, the study of the oscillatory activity revealed an apparent inability of the cortical circuits to produce correct activity patterns. Moreover, the fast spiking (FS) inhibitory GABAergic interneurons exhibited several abnormalities regarding the size of the action potentials, the threshold for spike firing, the time course of the action potential after-hyperpolarization (AHP), the firing frequency, and the frequency and peak amplitude of spontaneous excitatory postsynaptic currents (sEPSC’s). These morphological and functional alterations in the cortical inhibitory system characterize the Lis1/sLis1 mouse as a model of mild lissencephaly, showing a phenotype less drastic than the typical phenotype attributed to classical lissencephaly. Therefore, the results described in the present manuscript corroborate the idea that mutations in some regions of the Lis1 gene can produce phenotypes more similar to those typically described in schizophrenic and autistic patients and animal models.

Electroencephalography studies in schizophrenia reported impairments in circadian rhythm and oscillatory activity, which may reflect the deficits in cognitive and sensory processing. The current study evaluated the circadian rhythm and the state-dependent oscillatory pattern in control Wistar and a multiple hit schizophrenia rat model (Wisket) using custom-made software for identification of the artifacts and the classification of sleep-wake stages and the active and quiet awake substages. The Wisket animals have a clear light-dark cycle similar to controls, and their sleep-wake rhythm showed only a tendency to spend more time in non-rapid eye movement (NREM) and less in rapid eye movement (REM) stages. In spite of the weak diurnal variation in oscillation in both groups, the Wisket rats had higher power in the low-frequency delta, alpha, and beta bands and lower power in the high-frequency theta and gamma bands in most stages. Furthermore, the significant differences between the two groups were pronounced in the active waking substage. These data suggest that the special changes in the oscillatory pattern of this schizophrenia rat model may have a significant role in the impaired cognitive functions observed in previous studies. [ABSTRACT FROM AUTHOR]

A few studies have indicated that males and females respond differently to whole-body vibration (WBV) training. However, the existing insights are still insufficient and they cannot be transferred to sex-specific practice planning. To evaluate the effect of 5-week WBV training on neuromuscular [countermovement jump (CMJ), squat jump (SJ)] and cardiovascular [heart rate and blood pressure] data, taking into account sex-specific effects. This is a comparative experimental study including 96 healthy adults, divided into two groups: a WBV group (25 females and 24 males) and a control group (27 females and 20 males). The participants attended nine to ten training sessions (twice a week for 5 weeks), each lasting approximately 30 min. Both groups performed the same exercise routine on the vibration training device. For the WBV group, the training device was vibrating during the whole training session, including the breaks. For the control group, it was turned off. Maximum jump height (H, cm) and maximum relative power (MRP, kW/kg) were noted during CMJ and SJ performed on a force plate. Resting (sitting) heart rate (bpm) and blood pressure (mmHg) were measured twice, before and after the intervention. For each parameter, Δdata (= before - after) was calculated. Interactive effects of sex (2) vs group (2) vs session (2) were noted only in males and they only concerned ΔSJMPR and ΔCMJH: compared to the control group, the WBV group had better ΔSJMPR (1.39 ± 3.05 vs -2.69 ± 4.49 kW/kg, respectively) and ΔCMJH (0.50 ± 6.14 vs -4.42 ± 5.80 cm, respectively). No sex-specific effect of WBV on neuromuscular (CMJ and SJ) or cardiovascular (heart rate and blood pressure) data was found. [ABSTRACT FROM AUTHOR]

Electroencephalography studies in schizophrenia reported impairments in circadian rhythm and oscillatory activity, which may reflect the deficits in cognitive and sensory processing. The current study evaluated the circadian rhythm and the state-dependent oscillatory pattern in control Wistar and a multiple hit schizophrenia rat model (Wisket) using custom-made software for identification of the artifacts and the classification of sleep-wake stages and the active and quiet awake substages. The Wisket animals have a clear light-dark cycle similar to controls, and their sleep-wake rhythm showed only a tendency to spend more time in non-rapid eye movement (NREM) and less in rapid eye movement (REM) stages. In spite of the weak diurnal variation in oscillation in both groups, the Wisket rats had higher power in the low-frequency delta, alpha, and beta bands and lower power in the high-frequency theta and gamma bands in most stages. Furthermore, the significant differences between the two groups were pronounced in the active waking substage. These data suggest that the special changes in the oscillatory pattern of this schizophrenia rat model may have a significant role in the impaired cognitive functions observed in previous studies.

Neurons in the prefrontal cortex (PFC) encode sensory and context information, as well as sensory dominance in context-dependent decision-making [...]

During childhood, the body undergoes rapid changes suggesting the need to constantly update body representation based on the integration of multisensory signals. Sensory experiences in critical periods of early development may have a significant impact on the neurobiological mechanisms underpinning the development of the sense of one's own body. Specifically, preterm children are at risk for sensory processing difficulties, which may lead to specific vulnerability in binding together sensory information in order to modulate the representation of the bodily self. The present study aims to investigate the malleability of body ownership in preterm (N = 21) and full-term (N = 19) school-age children, as reflected by sensitivity to the Rubber Hand Illusion. The results revealed that multisensory processes underlying the ability to identify a rubber hand as being part of one's own body are already established in childhood, as indicated by a higher subjective feeling of embodiment over the rubber hand during synchronous visual-tactile stimulation. Notably, the effect of visual-tactile synchrony was related to the suppression of the alpha band oscillations over frontal, central, and parietal scalp regions, possibly indicating a greater activation of somatosensory and associative areas underpinning the illusory body ownership. Moreover, an interaction effect between visual-tactile condition and group emerged, suggesting that preterm children showed a greater suppression of alpha oscillatory activity during the illusion. This result together with lower scores of subjective embodiment over the rubber hand reported by preterm children indicate that preterm birth may affect the development of the flexible representation of the body. These findings provide an essential contribution to better understand the processes of identification and differentiation of the bodily self from the external environment, in both full-term and preterm children, paving the way for a multisensory and embodied approach to the investigation of social and cognitive development. [ABSTRACT FROM AUTHOR]

Summary: Drinking behavior in rodents is characterized by stereotyped, rhythmic licking movement, which is regulated by the basal ganglia. It is unclear how direct and indirect pathways control the lick bout and individual spout contact. We find that inactivating D1 and D2 receptor-expressing medium spiny neurons (MSNs) in the ventrolateral striatum (VLS) oppositely alters the number of licks in a bout. D1- and D2-MSNs exhibit different patterns of lick-sequence-related activity and different phases of oscillation time-locked to the lick cycle. On the timescale of a lick cycle, transient inactivation of D1-MSNs during tongue protrusion reduces spout contact probability, whereas transiently inactivating D2-MSNs has no effect. On the timescale of a lick bout, inactivation of D1-MSNs (D2-MSNs) causes rate increase (decrease) in a subset of basal ganglia output neurons that decrease firing during licking. Our results reveal the distinct roles of D1- and D2-MSNs in regulating licking at both coarse and fine timescales.

During childhood, the body undergoes rapid changes suggesting the need to constantly update body representation based on the integration of multisensory signals. Sensory experiences in critical periods of early development may have a significant impact on the neurobiological mechanisms underpinning the development of the sense of one’s own body. Specifically, preterm children are at risk for sensory processing difficulties, which may lead to specific vulnerability in binding together sensory information in order to modulate the representation of the bodily self. The present study aims to investigate the malleability of body ownership in preterm (N = 21) and full-term (N = 19) school-age children, as reflected by sensitivity to the Rubber Hand Illusion. The results revealed that multisensory processes underlying the ability to identify a rubber hand as being part of one’s own body are already established in childhood, as indicated by a higher subjective feeling of embodiment over the rubber hand during synchronous visual-tactile stimulation. Notably, the effect of visual-tactile synchrony was related to the suppression of the alpha band oscillations over frontal, central, and parietal scalp regions, possibly indicating a greater activation of somatosensory and associative areas underpinning the illusory body ownership. Moreover, an interaction effect between visual-tactile condition and group emerged, suggesting that preterm children showed a greater suppression of alpha oscillatory activity during the illusion. This result together with lower scores of subjective embodiment over the rubber hand reported by preterm children indicate that preterm birth may affect the development of the flexible representation of the body. These findings provide an essential contribution to better understand the processes of identification and differentiation of the bodily self from the external environment, in both full-term and preterm children, paving the way for a multisensory and embodied approach to the investigation of social and cognitive development.

Hepatic encephalopathy (HE) is a frequent neuropsychiatric complication in patients with acute or chronic liver failure. Symptoms of HE in particular include disturbances of sensory and motor functions and cognition. HE is triggered by heterogeneous factors such as ammonia being a main toxin, benzodiazepines, proinflammatory cytokines and hyponatremia. HE in patients with liver cirrhosis is triggered by a low-grade cerebral edema and cerebral oxidative/nitrosative stress which bring about a number of functionally relevant alterations including posttranslational protein modifications, oxidation of RNA, gene expression changes and senescence. These alterations are suggested to impair astrocyte/neuronal functions and communication. On the system level, a global slowing of oscillatory brain activity and networks can be observed paralleling behavioral perceptual and motor impairments. Moreover, these changes are related to increased cerebral ammonia, alterations in neurometabolite and neurotransmitter concentrations and cortical excitability in HE patients. [ABSTRACT FROM AUTHOR]

Abstract Background Pathophysiological concepts in delirium are not sufficient to define objective biomarkers suited to improve clinical approaches. Advances in neuroimaging have revalued electroencephalography (EEG) as a tool to assess oscillatory network activity in neuropsychiatric disease. Yet, research in the field is limited to small populations and largely confined to postoperative delirium, which impedes generalizability of findings and planning of prospective studies in other populations. This study aimed to assess effect sizes of connectivity measures in a large mixed population to demonstrate that there are measurable EEG differences between delirium and control patients. Methods This retrospective pilot study investigated EEG measures as biomarkers in delirium using a case-control design including patients diagnosed with delirium (DSM-5 criteria) and age-/gender-matched controls drawn from a database of 9980 patients (n = 129 and 414, respectively). Assessors were not blinded for groups. Power spectra and connectivity estimates, using the weighted phase log index, of continuous EEG data were compared between conditions. Alterations of information flow through nodes of intrinsic connectivity networks (ICN; default mode, salience, and executive control network) were evaluated in source space using betweenness centrality. This was done frequency specific and network nodes were defined by the multimodal human cerebral cortex parcellation based on human connectome project data. Results Delirium and control patients exhibited distinct EEG power, connectivity, and network characteristics (F (72,540) = 70.3, p

Patients with posterior cortical atrophy (PCA-AD) show more severe visuospatial and perceptual deficits than those with typical AD (tAD). The aim of this study was to investigate whether functional alterations measured by electroencephalography can help understand the mechanisms that explain this clinical heterogeneity. 21-channel electroencephalography recordings of 29 patients with PCA-AD were compared with 29 patients with tAD and 29 controls matched for age, gender, and disease severity. Patients with PCA-AD and tAD both showed a global decrease in fast and increase in slow oscillatory activity compared with controls. This pattern was, however, more profound in patients with PCA-AD which was driven by more extensive slowing of the posterior regions. Alpha band functional connectivity showed a similar decrease in PCA-AD and tAD. Compared with controls, a less integrated network topology was observed in PCA-AD, with a decrease of posterior and an increase of frontal hubness. In PCA-AD, decreased right parietal peak frequency correlated with worse performance on visual tasks. Regional vulnerability of the posterior network might explain the atypical pattern of neurodegeneration in PCA-AD. • PCA-AD subjects show more profound posterior oscillatory slowing compared to typical AD. • Right parietal peak frequency correlates with visual performance in PCA-AD. • PCA-AD functional networks show a decrease of posterior and increase of frontal hubness. [ABSTRACT FROM AUTHOR]

Sensory gating (SG) is a neurophysiological phenomenon whereby the response to the second stimulus in a repetitive pair is attenuated. This filtering of irrelevant or redundant information is thought to preserve neural resources for more behaviorally-relevant stimuli and thereby reflect the functional inhibition of sensory input. Developing a SG paradigm in which optimal suppression of sensory input is achieved requires investigators to consider numerous parameters such as stimulus intensity, time between stimulus pairs, and the inter-stimulus interval (ISI) within each pair. While these factors have been well defined for the interrogation of auditory gating, the precise parameters for eliciting optimal gating in the somatosensory domain are far less understood. To address this, we investigated the impact of varying the ISI within each identical pair of stimuli on gating using magnetoencephalography (MEG). Specifically, 25 healthy young adults underwent paired-pulse electrical stimulation of the median nerve with increasing ISIs between 100 and 1000 ​ms (in 100 ​ms increments). Importantly, for correspondence with previous studies of somatosensory gating, both time-domain and oscillatory neural responses to somatosensory stimulation were evaluated. Our results indicated that gating of somatosensory input was optimal (i.e., best suppression) for trials with an ISI of 200–220 ​ms, as evidenced by the smallest gating ratios and through statistical modeling estimations of optimal suppression. Importantly, this was true irrespective of whether oscillatory or evoked neural activity was used to calculate SG. Interestingly, oscillatory metrics of gating calculated using peak gamma (30-75 ​Hz) power and frequency revealed more robust gating (i.e., smaller ratios) than those calculated using time-domain neural responses, suggesting that high frequency oscillations may provide a more sensitive measure of SG. These findings have important implications for the development of optimal protocols and analysis pipelines to interrogate SG and inhibitory processing with a higher degree of sensitivity and accuracy.

Insights on the neurocognitive particularities of expert individuals have benefited from language studies on professional simultaneous interpreters (PSIs). Accruing research indicates that behavioral advantages in this population are restricted to those skills that are directly taxed during professional practice (e.g., translation as opposed to reading), but little is known about the neural signatures of such selective effects. To illuminate the issue, we recruited 17 PSIs and 15 non-interpreter bilinguals and compared behavioral and electrophysiological markers of word reading and translation from and into their native and non-native languages (L1 and L2, respectively). PSIs exhibited greater delta-theta (1–8 ​Hz) power across all tasks over varying topographies, but these were accompanied by faster performance only in the case of translation conditions. Moreover, neural differences in PSIs were most marked for L2-L1 translation (the dominant interpreting direction in their market), which exhibited maximally widespread modulations that selectively correlated with behavioral outcomes. Taken together, our results suggest that interpreting experience involves distinct neural signatures across reading and translation mechanisms, but that these are systematically related with processing efficiency only in domains that face elevated demands during everyday practice (i.e., L2-L1 translation). These findings can inform models of simultaneous interpreting, in particular, and expert cognitive processing, in general.

The cerebellum is strongly implicated in learning new motor skills. Theta burst stimulation (TBS), a form of repetitive transcranial magnetic stimulation, can be used to influence cerebellar activity. Our aim was to explore the potential of cerebellar TBS in modulating visuo-motor adaptation, a form of motor learning, in young healthy subjects. Cerebellar TBS was applied immediately before the learning phase of a visuo-motor adaptation task (VAT), in two different experiments. Firstly, we evaluated the behavioral effects of continuous (cTBS), intermittent (iTBS) or sham TBS on the learning, re-adaptation and de-adaptation phases of VAT. Subsequently, we investigated the changes induced by iTBS or sham TBS on motor cortical activity related to each phase of VAT, as measured by concomitant TMS/EEG recordings. We found that cerebellar TBS induced a robust bidirectional modulation of the VAT performance. More specifically, cerebellar iTBS accelerated visuo-motor adaptation, by speeding up error reduction in response to a novel perturbation. This gain of function was still maintained when the novel acquired motor plan was tested during a subsequent phase of re-adaptation. On the other hand, cerebellar cTBS induced the opposite effect, slowing the rate of error reduction in both learning and re-adaptation phases. Additionally, TMS/EEG recordings showed that cerebellar iTBS induced specific changes of cortical activity in the interconnected motor networks. The improved performance was accompanied by an increase of TMS-evoked cortical activity and a generalized desynchronization of TMS-evoked cortical oscillations. Taken together, our behavioral and neurophysiological findings provide the first-time multimodal evidence of the potential efficacy of cerebellar TBS in improving motor learning, by promoting successful cerebellar-cortical reorganization.

Abstract Background The cardinal features of Parkinson’s disease (PD) are bradykinesia, rigidity and rest tremor. Abnormal activity in the basal ganglia is predicted to underlie the mechanism of motor symptoms. This study aims to characterize properties of oscillatory activity in the basal ganglia and motor thalamus in patients with PD. Methods Twenty-nine patients with PD who underwent bilateral or unilateral electrode implantation for subthalamic nucleus (STN) DBS (n = 11), unilateral pallidotomy (n = 9) and unilateral thalamotomy (n = 9) were studied. Microelectrode recordings in the STN, globus pallidus internus (GPi) and ventral oral posterior/ventral intermediate of thalamus (Vop/Vim) were performed. Electromyography of the contralateral limbs was recorded. Single unit characteristics including interspike intervals were analyzed. Spectral and coherence analyses were assessed. Mean spontaneous firing rate (MSFR) of neurons was calculated. Analysis of variance and X2 test were performed. Results Of 76 STN neurons, 39.5% were 4–6 Hz band oscillatory neurons and 28.9% were β frequency band (βFB) oscillatory neurons. The MSFR was 44.2 ± 7.6 Hz. Of 62 GPi neurons, 37.1% were 4–6 Hz band oscillatory neurons and 27.4% were βFB neurons. The MSFR was 80.9 ± 9.6 Hz. Of 44 Vop neurons, 65.9% were 4–6 Hz band oscillatory neurons and 9% were βFB neurons. The MSFR was 24.4 ± 4.2 Hz. Of 30 Vim oscillatory neurons, 70% were 4–6 Hz band oscillatory neurons and 13.3% were βFB neurons. The MSFR was 30.3 ± 3.6 Hz. Further analysis indicated that proportion of βFB oscillatory neurons in STN and GPi was higher than that of similar neurons in the Vop and Vim (P

Background and Purpose: l-DOPA-induced dyskinesia (LID) is considered a major complication in the treatment of Parkinson's disease (PD). Buspirone (5-HT1A partial agonist) have shown promising results in the treatment of PD and LID, however no 5-HT-based treatment has been approved in PD. The present study was aimed to investigate how the substantia nigra pars reticulata (SNr) is affected by buspirone and whether it is a good target to study 5-HT antidyskinetic treatments.Experimental Approach: Buspirone was studied using in vivo single-unit, electrocorticogram, local field potential recordings along with microdialysis and immunohistochemistry in naïve/sham, 6-hydroxydopamine (6-OHDA)-lesioned or 6-OHDA-lesioned and l-DOPA-treated (6-OHDA/l-DOPA) rats.Key Results: Local buspirone inhibited SNr neuron activity in all groups. However, systemic buspirone reduced burst activity in 6-OHDA-lesioned rats (with or without l-DOPA treatment), whereas 8-OH-DPAT, a full 5-HT1A agonist induced larger inhibitory effects in sham animals. Neither buspirone nor 8-OH-DPAT markedly modified the low-frequency oscillatory activity in the SNr or synchronization within the SNr with the cortex. In addition, local perfusion of buspirone increased GABA and glutamate release in the SNr of naïve and 6-OHDA-lesioned rats but no effect in 6-OHDA/l-DOPA rats. In the 6-OHDA/l-DOPA group, increased 5-HT transporter and decreased 5-HT1A receptor expression was found.Conclusions and Implications: The effects of buspirone in SNr are influenced by dopamine loss and l-DOPA treatment. The present results suggest that the regulation of burst activity of the SNr induced by DA loss may be a good target to test new drugs for the treatment of PD and LID. [ABSTRACT FROM AUTHOR]

• Transcranial Static Magnetic Stimulation (tSMS) can modulate cortical excitability by acting on the oscillatory activity. • tSMS may alter motor learning through modulating cortical excitability. • Neuromodulation induced by tSMS may be a useful clinical tool for the treatment. Non-invasive brain stimulation (NIBS) techniques are extensively applied for the treatment of neuropsychiatric disorders and offer a powerful tool for addressing fundamental questions in neuroscience research. Recently, the use of static magnetic fields (SMFs) as a tool of NIBS has led to the development of a safe and promising method of neuromodulation called transcranial static magnetic stimulation (tSMS). However, the neurophysiological mechanisms regarding the effect of tSMS on the cortical elements are not yet fully understood. Here, we focus on the modulation of cortical excitability and oscillatory brain activity induced by tSMS. We believe that understanding the physiological mechanisms of this novel method is an important step for developing these techniques into potentially useful tools for the treatment of specific patient groups. Reviewing the neurophysiological evidence provided by human and animal studies suggests that tSMS may affect brain oscillations and alter behavioral parameters through the modulation of cortical excitability. In this review, we outline possible accounts and future directions to better understand the link between neural modification and accompanied behavioral changes. [ABSTRACT FROM AUTHOR]

• The wake-sleep transition is characterized by progressive local EEG modifications. • Sleep deprivation enhances the EEG changes that characterize the sleep onset. • The local EEG features of the sleep onset can be promoted by tCS protocols. • tCS can also be used to reduce sleepiness, but electrophysiological evidence is scarce. The sleep onset (SO) process is characterized by gradual electroencephalographic (EEG) changes. The interest for the possibility to manipulate the electrophysiological pattern of the wake-sleep transition is recently growing. This review aims to describe the EEG modifications of the SO process in healthy humans and the evidence about their experimental manipulation. We provide an overview of the electrophysiological changes during the wake-sleep transition, considering several methods to study the EEG signals. We then describe the impact of sleep deprivation (SD) on the electrophysiology of SO. Finally, we discuss the evidence about the possibility to modulate the local EEG activity through transcranial current stimulation protocols with the aim to promote, hinder, or manipulate the electrophysiological mechanisms of the wake-sleep transition. The reviewed findings highlight the local nature of the EEG processes during the SO and their intensification and speedup after SD. The evidence about the possibility to non-invasively affect the EEG pattern of the wake-sleep transition may have important implications for clinical conditions that would benefit from its prevention or promotion. [ABSTRACT FROM AUTHOR]

Background: Neurophysiological measures of brain function, such as magnetoencephalography (MEG), are widely used in clinical neurology and have strong relations with cognitive impairment and dementia but are still underdeveloped in multiple sclerosis (MS). Objectives: To demonstrate the value of clinically applicable MEG-measures in evaluating cognitive impairment in MS. Methods: In eyes-closed resting-state, MEG data of 83 MS patients and 34 healthy controls (HCs) peak frequencies and relative power of six canonical frequency bands for 78 cortical and 10 deep gray matter (DGM) areas were calculated. Linear regression models, correcting for age, gender, and education, assessed the relation between cognitive performance and MEG biomarkers. Results: Increased alpha1 and theta power was strongly associated with impaired cognition in patients, which differed between cognitively impaired (CI) patients and HCs in bilateral parietotemporal cortices. CI patients had a lower peak frequency than HCs. Oscillatory slowing was also widespread in the DGM, most pronounced in the thalamus. Conclusion: There is a clinically relevant slowing of neuronal activity in MS patients in parietotemporal cortical areas and the thalamus, strongly related to cognitive impairment. These measures hold promise for the application of resting-state MEG as a biomarker for cognitive disturbances in MS in a clinical setting. [ABSTRACT FROM AUTHOR]