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Brain stimulation can be used to engage and modulate rhythmic activity in brain networks. However, the outcomes of brain stimulation are shaped by behavioral states and endogenous fluctuations in brain activity. To better understand how this intrinsic oscillatory activity controls the susceptibility of the brain to stimulation, we analyzed a computational model of the thalamo-cortical system in two distinct states (rest and task-engaged) to identify the mechanisms by which endogenous alpha oscillations (8Hz–12Hz) are modulated by periodic stimulation. Our analysis shows that the different responses to stimulation observed experimentally in these brain states can be explained by a passage through a bifurcation combined with stochastic resonance — a mechanism by which irregular fluctuations amplify the response of a nonlinear system to weak periodic signals. Indeed, our findings suggest that modulation of brain oscillations is best achieved in states of low endogenous rhythmic activity, and that irregular state-dependent fluctuations in thalamic inputs shape the susceptibility of cortical population to periodic stimulation.

Arousal results in widespread activation of brain areas to increase their response in task and behavior relevant ways. Mediated by the Ascending Reticular Arousal System (ARAS), arousal-dependent inputs interact with neural circuitry to shape their dynamics. In the occipital cortex, such inputs may trigger shifts between dominant oscillations, where α activity is replaced by γ activity, or vice versa. A salient example of this are spectral power alternations observed while eyes are opened and/or closed. These transitions closely follow fluctuations in arousal, suggesting a common origin. To better understand the mechanisms at play, we developed and analyzed a computational model composed of two modules: a thalamocortical feedback circuit coupled with a superficial cortical network. Upon activation by noise-like inputs originating from the ARAS, our model is able to demonstrate that noise-driven non-linear interactions mediate transitions in dominant peak frequency, resulting in the simultaneous suppression of α limit cycle activity and the emergence of γ oscillations through coherence resonance. Reduction in input provoked the reverse effect - leading to anticorrelated transitions between α and γ power. Taken together, these results shed a new light on how arousal shapes oscillatory brain activity.

Cloud-affected radiances from geostationary satellite sensors provide the first area-wide observable signal of convection with high spatial resolution in the range of kilometers and high temporal resolution in the range of minutes. However, these observations are not yet assimilated in operational convection-resolving weather prediction models as the rapid, nonlinear evolution of clouds makes the assimilation of related observations very challenging. To address these challenges, we investigate the assimilation of satellite radiances from visible and infrared channels in idealized observing system simulation experiments (OSSEs) for a day with summertime deep convection in central Europe. This constitutes the first study assimilating a combination of all-sky observations from infrared and visible satellite channels, and the experiments provide the opportunity to test various assimilation settings in an environment where the observation forward operator and the numerical model exhibit no systematic errors. The experiments provide insights into appropriate settings for the assimilation of cloud-affected satellite radiances in an ensemble data assimilation system and demonstrate the potential of these observations for convective-scale weather prediction. Both infrared and visible radiances individually lead to an overall forecast improvement, but best results are achieved with a combination of both observation types that provide complementary information on atmospheric clouds. This combination strongly improves the forecast of precipitation and other quantities throughout the whole range of 8-h lead time.

Oscillatory brain activity is believed to play a central role in neural coding. Accumulating evidence shows that features of these oscillations are highly dynamic: power, frequency and phase fluctuate alongside changes in behavior and task demands. The role and mechanism supporting this variability is however poorly understood. We here analyze a network of recurrently connected spiking neurons with time delay displaying stable synchronous dynamics. Using mean-field and stability analyses, we investigate the influence of dynamic inputs on the frequency of firing rate oscillations. We show that afferent noise, mimicking inputs to the neurons, causes smoothing of the system's response function, displacing equilibria and altering the stability of oscillatory states. Our analysis further shows that these noise-induced changes cause a shift of the peak frequency of synchronous oscillations that scales with input intensity, leading the network towards critical states. We lastly discuss the extension of these principles to periodic stimulation, in which externally applied driving signals can trigger analogous phenomena. Our results reveal one possible mechanism involved in shaping oscillatory activity in the brain and associated control principles.

In recent years, more and more surgeries under general anesthesia have been performed with the assistance of electroencephalogram (EEG) monitors. An increase in anesthetic concentration leads to characteristic changes in the power spectra of the EEG. Although tracking the anesthetic-induced changes in EEG rhythms can be employed to estimate the depth of anesthesia, their precise underlying mechanisms are still unknown. A prominent feature in the EEG of some patients is the emergence of a strong power peak in the β-frequency band, which moves to the α-frequency band while increasing the anesthetic concentration. This feature is called the beta-buzz. In the present study, we use a thalamo-cortical neural population feedback model to reproduce observed characteristic features in frontal EEG power obtained experimentally during propofol general anesthesia, such as this beta-buzz. First, we find that the spectral power peak in the α- and δ-frequency ranges depend on the decay rate constant of excitatory and inhibitory synapses, but the anesthetic action on synapses does not explain the beta-buzz. Moreover, considering the action of propofol on the transmission delay between cortex and thalamus, the model reveals that the beta-buzz may result from a prolongation of the transmission delay by increasing propofol concentration. A corresponding relationship between transmission delay and anesthetic blood concentration is derived. Finally, an analytical stability study demonstrates that increasing propofol concentration moves the systems resting state towards its stability threshold.

Mental disorders are among the top most demanding challenges in world-wide health. A large number of mental disorders exhibit pathological rhythms, which serve as the disorders characteristic biomarkers. These rhythms are the targets for neurostimulation techniques. Open-loop neurostimulation employs stimulation protocols, which are rather independent of the patients health and brain state in the moment of treatment. Most alternative closed-loop stimulation protocols consider real-time brain activity observations but appear as adaptive open-loop protocols, where e.g., pre-defined stimulation sets in if observations fulfil pre-defined criteria. The present theoretical work proposes a fully-adaptive closed-loop neurostimulation setup, that tunes the brain activities power spectral density (PSD) according to a user-defined PSD. The utilized brain model is non-parametric and estimated from the observations via magnitude fitting in a pre-stimulus setup phase. Moreover, the algorithm takes into account possible conduction delays in the feedback connection between observation and stimulation electrode. All involved features are illustrated on pathological α- and γ-rhythms known from psychosis. To this end, we simulate numerically a linear neural population brain model and a non-linear cortico-thalamic feedback loop model recently derived to explain brain activity in psychosis.

The disruption of coupling between brain areas has been suggested as the mechanism underlying loss of consciousness in anesthesia. This hypothesis has been tested previously by measuring the information transfer between brain areas, and by taking reduced information transfer as a proxy for decoupling. Yet, information transfer is a function of the amount of information available in the information source-such that transfer decreases even for unchanged coupling when less source information is available. Therefore, we reconsidered past interpretations of reduced information transfer as a sign of decoupling, and asked whether impaired local information processing leads to a loss of information transfer. An important prediction of this alternative hypothesis is that changes in locally available information (signal entropy) should be at least as pronounced as changes in information transfer. We tested this prediction by recording local field potentials in two ferrets after administration of isoflurane in concentrations of 0.0%, 0.5%, and 1.0%. We found strong decreases in the source entropy under isoflurane in area V1 and the prefrontal cortex (PFC)-as predicted by our alternative hypothesis. The decrease in source entropy was stronger in PFC compared to V1. Information transfer between V1 and PFC was reduced bidirectionally, but with a stronger decrease from PFC to V1. This links the stronger decrease in information transfer to the stronger decrease in source entropy-suggesting reduced source entropy reduces information transfer. This conclusion fits the observation that the synaptic targets of isoflurane are located in local cortical circuits rather than on the synapses formed by interareal axonal projections. Thus, changes in information transfer under isoflurane seem to be a consequence of changes in local processing more than of decoupling between brain areas. We suggest that source entropy changes must be considered whenever interpreting changes in information transfer as decoupling.

Myelin surrounds axonal membranes to increase the conduction velocity of nerve impulses and thus reduce communication delays in neural signaling. Changes in myelination alter the distribution of delays in neural circuits, but the implications for their operation are poorly understood. We present a joint computational and non-linear dynamical method to explain how myelin-induced changes in axonal conduction velocity impact the firing rate statistics and spectral response properties of recurrent neural networks. Using a network of spiking neurons with distributed conduction delays driven by a spatially homogeneous noise, we combined probabilistic and mean field approaches. These reveal that myelin implements a gain control mechanism while stabilizing neural dynamics away from oscillatory regimes. The effect of myelin-induced changes in conduction velocity on network dynamics was found to be more pronounced in presence of correlated stochastic stimuli. Further, computational and theoretical power spectral analyses reveal a paradoxical effect where the loss of myelin promotes oscillatory responses to broadband time-varying stimuli. Taken together, our findings show that myelination can play a fundamental role in neural computation and its impairment in myelin pathologies such as epilepsy and multiple sclerosis. Myelin accelerates neural signaling by increasing axonal conduction velocity, but its impact on network dynamics remains unclear. The authors show that myelination implements a gain control mechanism, stabilizing neural dynamics away from oscillatory regimes, offering insights into its role in neural computation and disease.

In the past decade, there has been a surge of interest in using patterned brain stimulation to manipulate cortical oscillations, in both experimental and clinical settings. But the relationship between stimulation waveform and its impact on ongoing oscillations remains poorly understood and severely restrains the development of new paradigms. To address some aspects of this intricate problem, we combine computational and mathematical approaches, providing new insights into the influence of waveform of both low and high-frequency stimuli on synchronous neural activity. Using a cellular-based cortical microcircuit network model, we performed numerical simulations to test the influence of different waveforms on ongoing alpha oscillations, and derived a mean-field description of stimulation-driven dynamics to better understand the observed responses. Our analysis shows that high-frequency periodic stimulation translates into an effective transformation of the neurons' response function, leading to waveform-dependent changes in oscillatory dynamics and resting state activity. Moreover, we found that randomly fluctuating stimulation linearizes the neuron response function while constant input moves its activation threshold. Taken together, our findings establish a new theoretical framework in which stimulation waveforms impact neural systems at the population-scale through non-linear interactions.