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G. Bard Ermentrout

Publications and source records attributed to G. Bard Ermentrout.

13 recordsLinked to original sources

Cross-scale excitability in networks of synaptically-coupled quadratic integrate-and-fire neurons

From the action potentials of neurons and cardiac cells to the amplification of calcium signals in oocytes, excitability is a hallmark of many biological signalling processes. In recent years, excitability in single cells has been related to multiple-timescale dynamics through canards, special solutions which determine the effective thresholds of the all-or-none responses. However, the emergence of excitability in large populations remains an open problem. Here, we show that the mechanism of excitability in large networks and mean-field descriptions of coupled quadratic integrate-and-fire (QIF) cells mirrors that of the individual components. We initially exploit the Ott-Antonsen ansatz to derive low-dimensional dynamics for the coupled network and use it to describe the structure of canards via slow periodic forcing. We demonstrate that the thresholds for onset and offset of population firing can be found in the same way as those of the single cell. We combine theoretical analysis and numerical computations to develop a novel and comprehensive framework for excitability in large populations, applicable not only to models amenable to Ott-Antonsen reduction, but also to networks without a closed-form mean-field limit, in particular sparse networks.

math.DS↗

BioSimulators: a central registry of simulation engines and services for recommending specific tools

Computational models have great potential to accelerate bioscience, bioengineering, and medicine. However, it remains challenging to reproduce and reuse simulations, in part, because the numerous formats and methods for simulating various subsystems and scales remain siloed by different software tools. For example, each tool must be executed through a distinct interface. To help investigators find and use simulation tools, we developed BioSimulators (https://biosimulators.org), a central registry of the capabilities of simulation tools and consistent Python, command-line, and containerized interfaces to each version of each tool. The foundation of BioSimulators is standards, such as CellML, SBML, SED-ML, and the COMBINE archive format, and validation tools for simulation projects and simulation tools that ensure these standards are used consistently. To help modelers find tools for particular projects, we have also used the registry to develop recommendation services. We anticipate that BioSimulators will help modelers exchange, reproduce, and combine simulations.

q-bio.QM↗

When is sync globally stable in sparse networks of identical Kuramoto oscillators?

Synchronization in systems of coupled Kuramoto oscillators may depend on their natural frequencies, coupling, and underlying networks. In this paper, we reduce the alternatives to only one by considering identical oscillators where the only parameter that is allowed to change is the underlying network. While such a model was analyzed over the past few decades by studying the size of the basin of attraction of the synchronized state on restricted families of graphs, here we address a qualitative question on general graphs. In an analogy to resistive networks with current sources, we describe an algorithm that produces initial conditions that are often outside of the basin of attraction of the synchronized state. In particular, if a graph allows a cyclic graph clustering with a sufficient number of clusters or contains a sufficiently long induced subpath without cut vertices of the graph then there is a non-synchronous stable phase-locked solution. Thus, we provide a partial answer to when the synchronized state is not globally stable.

nlin.AO↗

Noise-induced synchronization and anti-resonance in excitable systems; Implications for information processing in Parkinson's Disease and Deep Brain Stimulation

We study the statistical physics of a surprising phenomenon arising in large networks of excitable elements in response to noise: while at low noise, solutions remain in the vicinity of the resting state and large-noise solutions show asynchronous activity, the network displays orderly, perfectly synchronized periodic responses at intermediate level of noise. We show that this phenomenon is fundamentally stochastic and collective in nature. Indeed, for noise and coupling within specific ranges, an asymmetry in the transition rates between a resting and an excited regime progressively builds up, leading to an increase in the fraction of excited neurons eventually triggering a chain reaction associated with a macroscopic synchronized excursion and a collective return to rest where this process starts afresh, thus yielding the observed periodic synchronized oscillations. We further uncover a novel anti-resonance phenomenon: noise-induced synchronized oscillations disappear when the system is driven by periodic stimulation with frequency within a specific range. In that anti-resonance regime, the system is optimal for measures of information capacity. This observation provides a new hypothesis accounting for the efficiency of Deep Brain Stimulation therapies in Parkinson's disease, a neurodegenerative disease characterized by an increased synchronization of brain motor circuits. We further discuss the universality of these phenomena in the class of stochastic networks of excitable elements with confining coupling, and illustrate this universality by analyzing various classical models of neuronal networks. Altogether, these results uncover some universal mechanisms supporting a regularizing impact of noise in excitable systems, reveal a novel anti-resonance phenomenon in these systems, and propose a new hypothesis for the efficiency of high-frequency stimulation in Parkinson's disease.

nlin.AO↗

A multiple timescales approach to bridging spiking- and population-level dynamics

A rigorous bridge between spiking-level and macroscopic quantities is an on-going and well-developed story for asynchronously firing neurons, but focus has shifted to include neural populations exhibiting varying synchronous dynamics. Recent literature has used the Ott--Antonsen ansatz (2008) to great effect, allowing a rigorous derivation of an order parameter for large oscillator populations. The ansatz has been successfully applied using several models including networks of Kuramoto oscillators, theta models, and integrate-and-fire neurons, along with many types of network topologies. In the present study, we take a converse approach: given the mean field dynamics of slow synapses, predict the synchronization properties of finite neural populations. The slow synapse assumption is amenable to averaging theory and the method of multiple timescales. Our proposed theory applies to two heterogeneous populations of N excitatory n-dimensional and N inhibitory m-dimensional oscillators with homogeneous synaptic weights. We then demonstrate our theory using two examples. In the first example we take a network of excitatory and inhibitory theta neurons and consider the case with and without heterogeneous inputs. In the second example we use Traub models with calcium for the excitatory neurons and Wang-Buzs{á}ki models for the inhibitory neurons. We accurately predict phase drift and phase locking in each example even when the slow synapses exhibit non-trivial mean-field dynamics.

q-bio.NC↗

Scalar Reduction of a Neural Field Model with Spike Frequency Adaptation

We study a deterministic version of a one- and two-dimensional attractor neural network model of hippocampal activity first studied by Itskov et al 2011. We analyze the dynamics of the system on the ring and torus domain with an even periodized weight matrix, assum- ing weak and slow spike frequency adaptation and a weak stationary input current. On these domains, we find transitions from spatially localized stationary solutions ("bumps") to (periodically modulated) solutions ("sloshers"), as well as constant and non-constant velocity traveling bumps depending on the relative strength of external input current and adaptation. The weak and slow adaptation allows for a reduction of the system from a distributed partial integro-differential equation to a system of scalar Volterra integro-differential equations describing the movement of the centroid of the bump solution. Using this reduction, we show that on both domains, sloshing solutions arise through an Andronov-Hopf bifurcation and derive a normal form for the Hopf bifurcation on the ring. We also show existence and stability of constant velocity solutions on both domains using Evans functions. In contrast to existing studies, we assume a general weight matrix of Mexican-hat type in addition to a smooth firing rate function.

q-bio.NC↗

The Utility of Phase Models in Studying Neural Synchronization

Synchronized neural spiking is associated with many cognitive functions and thus, merits study for its own sake. The analysis of neural synchronization naturally leads to the study of repetitive spiking and consequently to the analysis of coupled neural oscillators. Coupled oscillator theory thus informs the synchronization of spiking neuronal networks. A crucial aspect of coupled oscillator theory is the phase response curve (PRC), which describes the impact of a perturbation to the phase of an oscillator. In neural terms, the perturbation represents an incoming synaptic potential which may either advance or retard the timing of the next spike. The phase response curves and the form of coupling between reciprocally coupled oscillators defines the phase interaction function, which in turn predicts the synchronization outcome (in-phase versus anti-phase) and the rate of convergence. We review the two classes of PRC and demonstrate the utility of the phase model in predicting synchronization in reciprocally coupled neural models. In addition, we compare the rate of convergence for all combinations of reciprocally coupled Class I and Class II oscillators. These findings predict the general synchronization outcomes of broad classes of neurons under both inhibitory and excitatory reciprocal coupling.

q-bio.NC↗

Interactions of Solitary Pulses of E. coli in a One-Dimensional Nutrient Gradient

We study an anomalous behavior observed in interacting E. coli populations. When two populations of E. coli are placed on opposite ends of a long channel with a supply of nutrient between them, they will travel as pulses toward one another up the nutrient gradient. We present experimental evidence that, counterintuitively, the two pulses will in some cases change direction and be- gin moving away from each other and the nutrient back toward the end of the channel from which they originated. Simulations of the Keller-Segel chemotaxis model reproduce the experimental results. To gain better insight to the phenomenon, we introduce a heuristic approximation to the spatial profile of each population in the Keller-Segel model to derive a system of ordinary differential equations approximating the temporal dynamics of its center of mass and width. This approximate model simplifies analysis of the global dynamics of the bacterial system and allows us to efficiently explore the qualitative behavior changes across variations of parameters, and thereby provides experimentally testable hypotheses about the mechanisms behind the turnaround behavior.

q-bio.CB↗

Finite-size and correlation-induced effects in Mean-field Dynamics

The brain's activity is characterized by the interaction of a very large number of neurons that are strongly affected by noise. However, signals often arise at macroscopic scales integrating the effect of many neurons into a reliable pattern of activity. In order to study such large neuronal assemblies, one is often led to derive mean-field limits summarizing the effect of the interaction of a large number of neurons into an effective signal. Classical mean-field approaches consider the evolution of a deterministic variable, the mean activity, thus neglecting the stochastic nature of neural behavior. In this article, we build upon two recent approaches that include correlations and higher order moments in mean-field equations, and study how these stochastic effects influence the solutions of the mean-field equations, both in the limit of an infinite number of neurons and for large yet finite networks. We introduce a new model, the infinite model, which arises from both equations by a rescaling of the variables and, which is invertible for finite-size networks, and hence, provides equivalent equations to those previously derived models. The study of this model allows us to understand qualitative behavior of such large-scale networks. We show that, though the solutions of the deterministic mean-field equation constitute uncorrelated solutions of the new mean-field equations, the stability properties of limit cycles are modified by the presence of correlations, and additional non-trivial behaviors including periodic orbits appear when there were none in the mean field. The origin of all these behaviors is then explored in finite-size networks where interesting mesoscopic scale effects appear. This study leads us to show that the infinite-size system appears as a singular limit of the network equations, and for any finite network, the system will differ from the infinite system.

math.DS↗

Dynamics of Limit Cycle Oscillator Subject to General Noise

The phase description is a powerful tool for analyzing noisy limit cycle oscillators. The method, however, has found only limited applications so far, because the present theory is applicable only to the Gaussian noise while noise in the real world often has non-Gaussian statistics. Here, we provide the phase reduction for limit cycle oscillators subject to general, colored and non-Gaussian, noise including heavy-tailed noise. We derive quantifiers like mean frequency, diffusion constant, and the Lyapunov exponent to confirm consistency of the result. Applying our results, we additionally study a resonance between the phase and noise.

cond-mat.stat-mech↗

Stochastic phase reduction for a general class of noisy limit cycle oscillators

We formulate a phase-reduction method for a general class of noisy limit cycle oscillators and find that the phase equation is parametrized by the ratio between time scales of the noise correlation and amplitude relaxation of the limit cycle. The equation naturally includes previously proposed and mutually exclusive phase equations as special cases. The validity of the theory is numerically confirmed. Using the method, we reveal how noise and its correlation time affect limit cycle oscillations.

nlin.AO↗

Comment on "Phase Reduction of Stochastic Limit Cycle Oscillators"

This is a comment on a recent paper by Yoshimura and Arai [Phys. Rev. Lett. 101, 154101 (2008)] on phase reduction of noisy limit-cycle oscillators, in which the authors claimed that the conventional phase stochastic differential equation used in previous studies does not give a proper approximation and proposed a modified phase equation. Here we point out that both phase equations are valid depending on the situation. We argue that the relative size of amplitude relaxation time and noise correlation time determines which of the two equations is appropriate in the white-noise limit. The conventional phase equation is also a proper approximation to noisy limit cycles with sufficiently fast amplitude relaxation, which can be used as a starting point for further analysis.

nlin.AO↗

Relating Neural Dynamics to Neural Coding

We demonstrate that two key theoretical objects used widely in Computational Neuroscience, the phase-resetting curve (PRC) from dynamics and the spike triggered average (STA) from statistical analysis, are closely related under a wide range of stimulus conditions. We prove that the STA is proportional to the derivative of the PRC. We compare these analytic results to numerical calculations for the Hodgkin-Huxley neuron and we apply the method to neurons in the olfactory bulb of mice. This observation allows us to relate the stimulus-response properties of a neuron to its dynamics, bridging the gap between dynamical and information theoretic approaches to understanding brain computations and facilitating the interpretation of changes in channels and other cellular properties as influencing the representation of stimuli.

q-bio.NC↗