scholarly journals Thalamic activity during scalp slow waves in humans

2021 ◽  
Author(s):  
Péter P. Ujma ◽  
Orsolya Szalárdy ◽  
Dániel Fabó ◽  
Loránd Erőss ◽  
Róbert Bódizs
Keyword(s):  
Cortical Neurons ◽  
Large Scale ◽  
Nrem Sleep ◽  
Alpha Activity ◽  
Slow Waves ◽  
Gamma Activity ◽  
Field Potentials ◽  
Thalamic Nuclei ◽  
Time Frequency ◽  
Scalp Eeg

AbstractSlow waves are major pacemakers of NREM sleep oscillations. While slow waves themselves are mainly generated by cortical neurons, it is not clear what role thalamic activity plays in the generation of some oscillations grouped by slow waves, and to what extent thalamic activity during slow waves is itself driven by corticothalamic inputs. To address this question, we simultaneously recorded both scalp EEG and local field potentials from six thalamic nuclei (bilateral anterior, mediodorsal and ventral anterior) in fifteen epileptic patients (age-range: 17-64 years, 7 females) undergoing Deep Brain Stimulation Protocol and assessed the temporal evolution of thalamic activity relative to scalp slow waves using time-frequency analysis. We found that thalamic activity in all six nuclei during scalp slow waves is highly similar to what is observed on the scalp itself. Slow wave downstates are characterized by delta, theta and alpha activity and followed by beta, high sigma and low sigma activity during subsequent upstates. Gamma activity in the thalamus is not significantly grouped by slow waves. Theta and alpha activity appeared first on the scalp, but sigma activity appeared first in the thalamus. These effects were largely independent from the scalp region in which SWs were detected and the precise identity of thalamic nuclei. Our results indicate that while small thalamocortical neuron assemblies may initiate cortical oscillations, especially in the sleep spindle range, the large-scale neuronal activity in the thalamus which is detected by field potentials is principally driven by global cortical activity, and thus it is highly similar to what is observed on the scalp.

Modeling Sleep and Wakefulness in the Thalamocortical System

2005 ◽  
Vol 93 (3) ◽  
pp. 1671-1698 ◽  
Author(s):  
Sean Hill ◽  
Giulio Tononi
Keyword(s):  
Cortical Neurons ◽  
Large Scale ◽  
Slow Waves ◽  
Slow Oscillation ◽  
Sleep Mode ◽  
Thalamic Nuclei ◽  
Slow Oscillations ◽  
Corticocortical Connections

When the brain goes from wakefulness to sleep, cortical neurons begin to undergo slow oscillations in their membrane potential that are synchronized by thalamocortical circuits and reflected in EEG slow waves. To provide a self-consistent account of the transition from wakefulness to sleep and of the generation of sleep slow waves, we have constructed a large-scale computer model that encompasses portions of two visual areas and associated thalamic and reticular thalamic nuclei. Thousands of model neurons, incorporating several intrinsic currents, are interconnected with millions of thalamocortical, corticothalamic, and both intra- and interareal corticocortical connections. In the waking mode, the model exhibits irregular spontaneous firing and selective responses to visual stimuli. In the sleep mode, neuromodulatory changes lead to slow oscillations that closely resemble those observed in vivo and in vitro. A systematic exploration of the effects of intrinsic currents and network parameters on the initiation, maintenance, and termination of slow oscillations shows the following. 1) An increase in potassium leak conductances is sufficient to trigger the transition from wakefulness to sleep. 2) The activation of persistent sodium currents is sufficient to initiate the up-state of the slow oscillation. 3) A combination of intrinsic and synaptic currents is sufficient to maintain the up-state. 4) Depolarization-activated potassium currents and synaptic depression terminate the up-state. 5) Corticocortical connections synchronize the slow oscillation. The model is the first to integrate intrinsic neuronal properties with detailed thalamocortical anatomy and reproduce neural activity patterns in both wakefulness and sleep, thereby providing a powerful tool to investigate the role of sleep in information transmission and plasticity.

Dynamic coupling among neocortical neurons during evoked and spontaneous spike-wave seizure activity

1994 ◽  
Vol 72 (5) ◽  
pp. 2051-2069 ◽  
Author(s):  
M. Steriade ◽  
F. Amzica
Keyword(s):  
Cortical Neurons ◽  
Time Course ◽  
Early Stage ◽  
Field Potential ◽  
Time Lags ◽  
Temporal Relations ◽  
Intracellular Recordings ◽  
Field Potentials ◽  
Thalamic Nuclei ◽  
Spike Wave

1. We investigated the development from patterns of electroencephalogram (EEG) synchronization to paroxysms consisting of spike-wave (SW) complexes at 2–4 Hz or to seizures at higher frequencies (7–15 Hz). We used multisite, simultaneous EEG, extracellular, and intracellular recordings from various neocortical areas and thalamic nuclei of anesthetized cats. 2. The seizures were observed in 25% of experimental animals, all maintained under ketamine and xylazine anesthesia, and were either induced by thalamocortical volleys and photic stimulation or occurred spontaneously. Out of unit and field potential recordings within 370 cortical and 65 thalamic sites, paroxysmal events occurred in 70 cortical and 8 thalamic sites (approximately 18% and 12%, respectively), within which a total of 181 neurons (143 extracellular and 38 intracellular) were simultaneously recorded in various combinations of cell groups. 3. Stimulus-elicited and spontaneous SW seizures at 2–4 Hz lasted for 15–35 s and consisted of barrages of action potentials related to the spiky depth-negative (surface-positive) field potentials, followed by neuronal silence during the depth-positive wave component of SW complexes. The duration of inhibitory periods progressively increased during the seizure, at the expense of the phasic excitatory phases. 4. Intracellular recordings showed that, during such paroxysms, cortical neurons displayed a tonic depolarization (approximately 10–20 mV), sculptured by rhythmic hyperpolarizations. 5. In all cases, measures of synchrony demonstrated time lags between discharges of simultaneously recorded cortical neurons, from as short as 3–10 ms up to 50 ms or even longer intervals. Synchrony was assessed by cross-correlograms, by a method termed first-spike-analysis designed to detect dynamic temporal relations between neurons and relying on the detection of the first action potential in a spike train, and by a method termed sequential-field-correlation that analyzed the time course of field potentials simultaneously recorded from different cortical areas. 6. The degree of synchrony progressively increased from preseizure sleep patterns to the early stage of the SW seizure and, further, to its late stage. In some cases the time relation between neurons during the early stages of seizures was inversed during late stages. 7. These data show that, although the common definition of SW seizures, regarded as suddenly generalized and bilaterally synchronous activities, may be valid at the macroscopic EEG level, cortical neurons display time lags between their rhythmic spike trains, progressively increased synchrony, and changes in the temporal relations between their discharges during the paroxysms.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Sleep spindles, ripples, and interictal epileptiform discharges in the human anterior and mediodorsal thalamus

2021 ◽  
Author(s):  
Orsolya Szalardy ◽  
Peter Simor ◽  
Peter Przemyslaw Ujma ◽  
Zsofia Jordan ◽  
Laszlo Halasz ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Nrem Sleep ◽  
Cortical Activity ◽  
Sleep Spindles ◽  
Time Frequency ◽  
Scalp Eeg ◽  
Epileptiform Discharges ◽  
Interictal Epileptiform Discharges ◽  
Human Thalamus ◽  
Result Show

Sleep spindles are major oscillatory components of Non-Rapid Eye Movement (NREM) sleep, reflecting hyperpolarization-rebound sequences of thalamocortical neurons, the inhibition of which is caused by the NREM-dependent activation of GABAergic neurons in the reticular thalamic nucleus. Reports suggest a link between sleep spindles and several forms of interictal epileptic discharges (IEDs) which are considered as expressions of pathological off-line neural plasticity in the central nervous system. Here we investigated the relationship between thalamic sleep spindles, IEDs and ripples in the anterior and mediodorsal nuclei (ANT and MD) of epilepsy patients. Whole-night LFP from the ANT and MD were co-registered with scalp EEG/polysomnography by using externalized leads in 15 epilepsy patients undergoing Deep Brain Stimulation protocol. Slow (~12 Hz) and fast (~14 Hz) sleep spindles were present in the human ANT and MD. Roughly, one third of thalamic sleep spindles were associated with IEDs or ripples. Both IED- and ripple-associated spindles were longer than pure spindles. IED-associated thalamic sleep spindles were characterized by broadband increase in thalamic and cortical activity, both below and above the spindle frequency range, whereas ripple-associated thalamic spindles exceeded pure spindles in terms of 80-200 Hz thalamic, but not cortical activity as indicated by time-frequency analysis. These result show that thalamic spindles coupled with IEDs are reflected at the scalp slow and beta-gamma oscillation as well. IED density during sleep spindles in the MD, but not in the ANT was identified as correlates of years spent with epilepsy, whereas no signs of pathological processes were correlated with measures of ripple and spindle association. Furthermore, the density of ripple-associated sleep spindles in the ANT showed a positive correlation with general intelligence. Our findings indicate the complex and multifaceted role of the human thalamus in sleep spindle-related physiological and pathological neural plasticity.

Spike-Wave Complexes and Fast Components of Cortically Generated Seizures. III. Synchronizing Mechanisms

1998 ◽  
Vol 80 (3) ◽  
pp. 1480-1494 ◽  
Author(s):  
Dag Neckelmann ◽  
Florin Amzica ◽  
Mircea Steriade
Keyword(s):  
Cortical Neurons ◽  
Time Delays ◽  
Slow Oscillation ◽  
Time Lags ◽  
Intracellular Recordings ◽  
Field Potentials ◽  
Thalamic Nuclei ◽  
Dorsal Thalamus ◽  
Cross Correlations ◽  
Spike Wave

Neckelmann, Dag, Florin Amzica, and Mircea Steriade. Spike-wave complexes and fast components of cortically generated seizures. III. Synchronizing mechanisms. J. Neurophysiol. 80: 1480–1494, 1998. The intracortical and thalamocortical synchronization of spontaneously occurring or bicuculline-induced seizures, consisting of spike-wave (SW) or polyspike-wave (PSW) complexes at 2–3 Hz and fast runs at 10–15 Hz, was investigated in cats under ketamine-xylazine anesthesia. We used single and dual simultaneous intracellular recordings from cortical areas 5 and 7, and extracellular recordings of unit firing and field potentials from neocortical areas 5, 7, 17, 18, as well as related thalamic nuclei. The evolution of time delays between paroxysmal depolarizing events in single neurons or neuronal pools recorded from adjacent and distant sites was analyzed by using 1) sequential cross-correlations between field potentials, 2) averaged activities triggered by the spiky component of cortical SW/PSW complexes, and 3) time histograms between neuronal discharges. In all instances, the paroxysmal activities recorded from the dorsal thalamus lagged the onset of seizures in neocortex. The time lags between simultaneously impaled cortical neurons were significantly smaller during SW complexes than during the prior epochs of slow oscillation. During seizures, as during the slow oscillation, the intracortical synchrony was reduced with increased distance between different cortical sites. Dual intracellular recordings showed that, during the same seizure, time lags were not constant and, instead, reflected alternating precession of the recorded foci. After transection between areas 5 and 7, the intracortical synchrony was lost, but corticothalamocortical volleys could partially restore seizure synchrony. These data show that the neocortex leads the thalamus during SW/PSW seizures, that time lags between cortical foci are not static, and that thalamus may assist synchronization of SW/PSW seizures after disconnection of intracortical synaptic linkages.

scholarly journals Sleep-like bistability, loss of causality and complexity in the brain of Unresponsive Wakefulness Syndrome patients

2018 ◽  
Author(s):  
M. Rosanova ◽  
M. Fecchio ◽  
S. Casarotto ◽  
S. Sarasso ◽  
A.G. Casali ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Decomposition Analysis ◽  
Silent Period ◽  
Nrem Sleep ◽  
Underlying Mechanism ◽  
Sensory Stimuli ◽  
Time Frequency ◽  
Frequency Decomposition ◽  
Global Brain ◽  
The Brain

AbstractUnresponsiveness Wakefulness Syndrome (UWS) patients may retain intact portions of the thalamocortical system that are spontaneously active and responsive to sensory stimuli. In these patients, Transcranial Magnetic Stimulation combined with electroencephalography (TMS/EEG) also reveals preserved cortical reactivity, but in most cases, the residual thalamocortical circuits fail to engage complex causal interactions, as assessed by the perturbational complexity index (PCI).Another condition during which thalamocortical circuits are intact, active and reactive, yet unable to generate complex responses, is physiological non-rapid eye movement (NREM) sleep. The underlying mechanism is bistability: the tendency of cortical neurons to fall into a silent period (OFF-period) upon receiving an input.Here we tested whether a pathological form of bistability may be responsible for loss of brain complexity in UWS patients. Time-frequency decomposition analysis of TMS/EEG responses in UWS patients revealed the occurrence of OFF-periods (detected as a transient suppression of high-frequency oscillations in the EEG) similar to the ones evoked by TMS in the cortex of healthy sleeping subjects. Pathological OFF-periods were detected in any cortical area, significantly impaired local causal interactions (as measured by PLF) and prevented the buildup of global complexity (as measured by PCI) in the brain of UWS patients.Our results draw a first link between neuronal events (OFF-periods) and global brain dynamics (complexity) in UWS patients. To the extent that sleep-like bistability represents the common functional endpoint of loss of complexity, detecting its presence and tracking its evolution over time, may offer a valuable read-out to devise, guide and titrate therapeutic strategies aimed at restoring consciousness.

Large-scale neocortical dynamics: Some EEG data analysis implications

2000 ◽  
Vol 23 (3) ◽  
pp. 401-402
Author(s):  
Richard E. Greenblatt
Keyword(s):  
Data Analysis ◽  
Frequency Distribution ◽  
Large Scale ◽  
Time Frequency ◽  
Scalp Eeg ◽  
Source Estimation ◽  
Eeg Data ◽  
Neocortical Dynamics ◽  
Distribution Matrix ◽  
Time Frequency Distribution

The spatial time-frequency distribution matrix and associated Rényi entropy is proposed as the basis for a method that may be useful for estimating the significance of nonlocal neocortical interactions in the analysis of scalp EEG data. Implications of nonlocal interactions for source estimation are also considered.

scholarly journals 0352 A Large-Scale EEG Study at Home to Objectivise Effects of Ageing on Slow Wave Sleep and Process S

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A133-A134
Author(s):  
K El Kanbi ◽  
V Thorey ◽  
L Artemis ◽  
A Chouraki ◽  
T Trichet ◽  
...  
Keyword(s):  
Slow Wave ◽  
Large Scale ◽  
Slow Wave Sleep ◽  
Large Population ◽  
Nrem Sleep ◽  
Slow Waves ◽  
High Signal ◽  
Eeg Signals ◽  
Sleep Complaints ◽  
Loop Procedure

Abstract Introduction Several studies have shown slow wave sleep (SWS) is altered with ageing. However, most of these studies have been conducted in-lab and usually over a single night. In this study, we assessed the evolution of process S with ageing by analysing the dynamics of endogenous and auditory-evoked slow waves in a large population. Methods 300 participants (200 M, 20 - 70 y.o.) were selected from volunteers users wearing a sleep headband for at least 3 nights, meeting the criteria of high signal quality and having no subjective sleep complaints nor being shift-workers. The Dreem headband is a connected device able to monitor EEG signals as well as pulse and movement and performs sleep staging in real-time automatically. Slow waves were detected as large negative deflections on the filtered EEG signals during NREM sleep. The auditory evoked slow waves were done using a previously validated closed-loop procedure. Results In our study, age was strongly correlated with N3 sleep duration (r=-0.34, p<0.0001), slow wave amplitude (r=-0.25, p<0.0001), and slow wave density (r=-0.40, p<0.0001). The slope of the slow wave activity, representing the process S here, was significantly decreased (r=-0.32, p<0.0001). This effect was mainly due to changes in the density of slow waves in the first 2 hours of sleep (r=-0.41, p<0.0001). Finally, our results show a decrease in the probability of auditory evoked slow waves (r=-0.43, p<0.0001). Conclusion These results confirmed the in-lab studies showing a heterogeneous alteration of homoeostatic process S with age, as well as a general decrease of slow wave occurrences, that is observed in parallel of a decrease of the probability of evoking slow waves, suggesting a global change in the system responsible for slow wave generation. Support This study was supported by Dreem sas and ANR, FLAG ERA 2015, HPB SLOW-Dyn

scholarly journals Synaptic refinement during development and its effect on slow-wave activity: a computational study

2016 ◽  
Vol 115 (4) ◽  
pp. 2199-2213 ◽  
Author(s):  
Erik P. Hoel ◽  
Larissa Albantakis ◽  
Chiara Cirelli ◽  
Giulio Tononi
Keyword(s):  
Experimental Data ◽  
Slow Wave ◽  
Cortical Neurons ◽  
Large Scale ◽  
Computational Study ◽  
Neural Model ◽  
Wave Activity ◽  
Spike Timing ◽  
Slow Waves ◽  
Slow Wave Activity

Recent evidence suggests that synaptic refinement, the reorganization of synapses and connections without significant change in their number or strength, is important for the development of the visual system of juvenile rodents. Other evidence in rodents and humans shows that there is a marked drop in sleep slow-wave activity (SWA) during adolescence. Slow waves reflect synchronous transitions of neuronal populations between active and inactive states, and the amount of SWA is influenced by the connection strength and organization of cortical neurons. In this study, we investigated whether synaptic refinement could account for the observed developmental drop in SWA. To this end, we employed a large-scale neural model of primary visual cortex and sections of the thalamus, capable of producing realistic slow waves. In this model, we reorganized intralaminar connections according to experimental data on synaptic refinement: during prerefinement, local connections between neurons were homogenous, whereas in postrefinement, neurons connected preferentially to neurons with similar receptive fields and preferred orientations. Synaptic refinement led to a drop in SWA and to changes in slow-wave morphology, consistent with experimental data. To test whether learning can induce synaptic refinement, intralaminar connections were equipped with spike timing-dependent plasticity. Oriented stimuli were presented during a learning period, followed by homeostatic synaptic renormalization. This led to activity-dependent refinement accompanied again by a decline in SWA. Together, these modeling results show that synaptic refinement can account for developmental changes in SWA. Thus sleep SWA may be used to track noninvasively the reorganization of cortical connections during development.

scholarly journals Regional low-frequency oscillations in human rapid-eye movement sleep

2018 ◽  
Author(s):  
Giulio Bernardi ◽  
Monica Betta ◽  
Emiliano Ricciardi ◽  
Pietro Pietrini ◽  
Giulio Tononi ◽  
...  
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Rem Sleep ◽  
Low Frequency ◽  
Nrem Sleep ◽  
Slow Waves ◽  
Gamma Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movements ◽  
Low Frequency Oscillations

AbstractAlthough the EEG slow wave of sleep is typically considered to be a hallmark of Non Rapid Eye Movement (NREM) sleep, recent work in mice has shown that slow waves can also occur in REM sleep. Here we investigated the presence and cortical distribution of low-frequency (1-4 Hz) oscillations in human REM sleep by analyzing high-density EEG sleep recordings obtained in 28 healthy subjects. We identified two clusters of low-frequency oscillations with distinctive properties: 1) a fronto-central cluster characterized by ∼2.5-3.0 Hz, relatively large, notched delta waves (so-called ‘sawtooth waves’) that tended to occur in bursts, were associated with increased gamma activity and rapid eye movements, and upon source modeling, displayed an occipito-temporal and a fronto-central component; and 2) a medial occipital cluster characterized by more isolated, slower (<2 Hz) and smaller waves that were not associated with rapid eye movements, displayed a negative correlation with gamma activity and were also found in NREM sleep. Thus, low-frequency oscillations are an integral part of REM sleep in humans, and the two identified subtypes (sawtooth and medial-occipital slow waves) may reflect distinct generation mechanisms and functional roles. Sawtooth waves, which are exclusive to REM sleep, share many characteristics with ponto-geniculo-occipital (PGO) waves described in animals and may represent the human equivalent or a closely related event while medio-occipital slow waves appear similar to NREM sleep slow waves.

scholarly journals Role of somatostatin-positive cortical interneurons in the generation of sleep slow waves

2017 ◽  
Author(s):  
Chadd M. Funk ◽  
Kayla Peelman ◽  
Michele Bellesi ◽  
William Marshall ◽  
Chiara Cirelli ◽  
...  
Keyword(s):  
Slow Wave ◽  
Cortical Neurons ◽  
Nrem Sleep ◽  
Slow Waves ◽  
Inhibitory Neurons ◽  
Excitatory Transmission ◽  
Cortical Interneurons ◽  
Somatic Inhibition ◽  
Apical Dendrites

SUMMARYCortical slow waves – the hallmark of NREM sleep - reflect near-synchronous OFF periods in cortical neurons. However, the mechanisms triggering such OFF periods are unclear, as there is little evidence for somatic inhibition. We studied cortical inhibitory interneurons that express somatostatin (SOM), because ∼70% of them are Martinotti cells that target diffusely layer 1 and can block excitatory transmission presynaptically, at glutamatergic terminals, and postsynaptically, at apical dendrites, without inhibiting the soma. In freely moving mice, we show that SOM+ cells can fire immediately before slow waves and their optogenetic stimulation triggers neuronal OFF periods during sleep. Next, we show that chemogenetic activation of SOM+ cells increases slow wave activity (SWA), the slope of individual slow waves, and the duration of NREM sleep; whereas their chemogenetic inhibition decreases SWA and slow wave incidence without changing time spent asleep. By contrast, activation of parvalbumin+ (PV+) cells, the most numerous population of cortical inhibitory neurons, greatly decreases SWA and cortical firing. These results indicate that SOM+ cells, but not PV+ cells, are involved in the generation of sleep slow waves. Whether Martinotti cells are solely responsible for this effect, or are complemented by other classes of inhibitory neurons, remains to be investigated.

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