Metastability in networks of nonlinear stochastic integrate-and-fire neurons.

Neurons in the brain continuously process the barrage of sensory inputs they receive from the environment. A wide array of experimental work has shown that the collective activity of neural populations encodes and processes this constant bombardment of information. How these collective patterns of activity depend on single neuron properties is often unclear. Single-neuron recordings have shown that individual neural responses to inputs are nonlinear, which prevents a straightforward extrapolation from single neuron features to emergent collective states. In this work, we use a field theoretic formulation of a stochastic leaky integrate-and-fire model to study the impact of nonlinear intensity functions on macroscopic network activity. We show that the interplay between nonlinear spike emission and membrane potential resets can i) give rise to metastable transitions between active firing rate states, and ii) can enhance or suppress mean firing rates and membrane potentials in opposite directions.

Statistically inferred neuronal connections in subsampled neural networks strongly correlate with spike train covariances.

Statistically inferred neuronal connections from observed spike train data are often skewed from ground truth by factors such as model mismatch, unobserved neurons, and limited data. Spike train covariances, sometimes referred to as "functional connections," are often used as a proxy for the connections between pairs of neurons, but reflect statistical relationships between neurons, not anatomical connections. Moreover, covariances are not causal: spiking activity is correlated in both the past and the future, whereas neurons respond only to synaptic inputs in the past. Connections inferred by maximum likelihood inference, however, can be constrained to be causal. However, we show in this work that the inferred connections in spontaneously active networks modeled by stochastic leaky integrate-and-fire networks strongly correlate with the covariances between neurons, and may reflect noncausal relationships, when many neurons are unobserved or when neurons are weakly coupled. This phenomenon occurs across different network structures, including random networks and balanced excitatory-inhibitory networks. We use a combination of simulations and a mean-field analysis with fluctuation corrections to elucidate the relationships between spike train covariances, inferred synaptic filters, and ground-truth connections in partially observed networks.

Applications of information geometry to spiking neural network activity.

The space of possible behaviors that complex biological systems may exhibit is unimaginably vast, and these systems often appear to be stochastic, whether due to variable noisy environmental inputs or intrinsically generated chaos. The brain is a prominent example of a biological system with complex behaviors. The number of possible patterns of spikes emitted by a local brain circuit is combinatorially large, although the brain may not make use of all of them. Understanding which of these possible patterns are actually used by the brain, and how those sets of patterns change as properties of neural circuitry change is a major goal in neuroscience. Recently, tools from information geometry have been used to study embeddings of probabilistic models onto a hierarchy of model manifolds that encode how model outputs change as a function of their parameters, giving a quantitative notion of "distances" between outputs. We apply this method to a network model of excitatory and inhibitory neural populations to understand how the competition between membrane and synaptic response timescales shapes the network's information geometry. The hyperbolic embedding allows us to identify the statistical parameters to which the model behavior is most sensitive, and demonstrate how the ranking of these coordinates changes with the balance of excitation and inhibition in the network.

Evolution of innate behavioral strategies through competitive population dynamics.

Many organism behaviors are innate or instinctual and have been "hard-coded" through evolution. Current approaches to understanding these behaviors model evolution as an optimization problem in which the traits of organisms are assumed to optimize an objective function representing evolutionary fitness. Here, we use a mechanistic birth-death dynamics approach to study the evolution of innate behavioral strategies in a simulated population of organisms. In particular, we performed agent-based stochastic simulations and mean-field analyses of organisms exploring random environments and competing with each other to find locations with plentiful resources. We find that when organism density is low, the mean-field model allows us to derive an effective objective function, predicting how the most competitive phenotypes depend on the exploration-exploitation trade-off between the scarcity of high-resource sites and the increase in birth rate those sites offer organisms. However, increasing organism density alters the most competitive behavioral strategies and precludes the derivation of a well-defined objective function. Moreover, there exists a range of densities for which the coexistence of many phenotypes persists for evolutionarily long times.

Dysregulation of excitatory neural firing replicates physiological and functional changes in aging visual cortex.

The mammalian visual system has been the focus of countless experimental and theoretical studies designed to elucidate principles of neural computation and sensory coding. Most theoretical work has focused on networks intended to reflect developing or mature neural circuitry, in both health and disease. Few computational studies have attempted to model changes that occur in neural circuitry as an organism ages non-pathologically. In this work we contribute to closing this gap, studying how physiological changes correlated with advanced age impact the computational performance of a spiking network model of primary visual cortex (V1). Our results demonstrate that deterioration of homeostatic regulation of excitatory firing, coupled with long-term synaptic plasticity, is a sufficient mechanism to reproduce features of observed physiological and functional changes in neural activity data, specifically declines in inhibition and in selectivity to oriented stimuli. This suggests a potential causality between dysregulation of neuron firing and age-induced changes in brain physiology and functional performance. While this does not rule out deeper underlying causes or other mechanisms that could give rise to these changes, our approach opens new avenues for exploring these underlying mechanisms in greater depth and making predictions for future experiments.

Predicting how and when hidden neurons skew measured synaptic interactions.

A major obstacle to understanding neural coding and computation is the fact that experimental recordings typically sample only a small fraction of the neurons in a circuit. Measured neural properties are skewed by interactions between recorded neurons and the "hidden" portion of the network. To properly interpret neural data and determine how biological structure gives rise to neural circuit function, we thus need a better understanding of the relationships between measured effective neural properties and the true underlying physiological properties. Here, we focus on how the effective spatiotemporal dynamics of the synaptic interactions between neurons are reshaped by coupling to unobserved neurons. We find that the effective interactions from a pre-synaptic neuron r' to a post-synaptic neuron r can be decomposed into a sum of the true interaction from r' to r plus corrections from every directed path from r' to r through unobserved neurons. Importantly, the resulting formula reveals when the hidden units have-or do not have-major effects on reshaping the interactions among observed neurons. As a particular example of interest, we derive a formula for the impact of hidden units in random networks with "strong" coupling-connection weights that scale with [Formula: see text], where N is the network size, precisely the scaling observed in recent experiments. With this quantitative relationship between measured and true interactions, we can study how network properties shape effective interactions, which properties are relevant for neural computations, and how to manipulate effective interactions.

How Do Efficient Coding Strategies Depend on Origins of Noise in Neural Circuits?

Neural circuits reliably encode and transmit signals despite the presence of noise at multiple stages of processing. The efficient coding hypothesis, a guiding principle in computational neuroscience, suggests that a neuron or population of neurons allocates its limited range of responses as efficiently as possible to best encode inputs while mitigating the effects of noise. Previous work on this question relies on specific assumptions about where noise enters a circuit, limiting the generality of the resulting conclusions. Here we systematically investigate how noise introduced at different stages of neural processing impacts optimal coding strategies. Using simulations and a flexible analytical approach, we show how these strategies depend on the strength of each noise source, revealing under what conditions the different noise sources have competing or complementary effects. We draw two primary conclusions: (1) differences in encoding strategies between sensory systems-or even adaptational changes in encoding properties within a given system-may be produced by changes in the structure or location of neural noise, and (2) characterization of both circuit nonlinearities as well as noise are necessary to evaluate whether a circuit is performing efficiently.

Probabilistic model of waiting times between large failures in sheared media.

Using a probabilistic approximation of a mean-field mechanistic model of sheared systems, we analytically calculate the statistical properties of large failures under slow shear loading. For general shear F(t), the distribution of waiting times between large system-spanning failures is a generalized exponential distribution, ρ_{T}(t)=λ(F(t))P(F(t))exp[-∫_{0}^{t}dτλ(F(τ))P(F(τ))], where λ(F(t)) is the rate of small event occurrences at stress F(t) and P(F(t)) is the probability that a small event triggers a large failure. We study the behavior of this distribution as a function of fault properties, such as heterogeneity or shear rate. Because the probabilistic model accommodates any stress loading F(t), it is particularly useful for modeling experiments designed to understand how different forms of shear loading or stress perturbations impact the waiting-time statistics of large failures. As examples, we study how periodic perturbations or fluctuations on top of a linear shear stress increase impact the waiting-time distribution.

Experiments and Model for Serration Statistics in Low-Entropy, Medium-Entropy, and High-Entropy Alloys.

High-entropy alloys (HEAs) are new alloys that contain five or more elements in roughly-equal proportion. We present new experiments and theory on the deformation behavior of HEAs under slow stretching (straining), and observe differences, compared to conventional alloys with fewer elements. For a specific range of temperatures and strain-rates, HEAs deform in a jerky way, with sudden slips that make it difficult to precisely control the deformation. An analytic model explains these slips as avalanches of slipping weak spots and predicts the observed slip statistics, stress-strain curves, and their dependence on temperature, strain-rate, and material composition. The ratio of the weak spots' healing rate to the strain-rate is the main tuning parameter, reminiscent of the Portevin-LeChatellier effect and time-temperature superposition in polymers. Our model predictions agree with the experimental results. The proposed widely-applicable deformation mechanism is useful for deformation control and alloy design.

Universal Quake Statistics: From Compressed Nanocrystals to Earthquakes.

Slowly-compressed single crystals, bulk metallic glasses (BMGs), rocks, granular materials, and the earth all deform via intermittent slips or "quakes". We find that although these systems span 12 decades in length scale, they all show the same scaling behavior for their slip size distributions and other statistical properties. Remarkably, the size distributions follow the same power law multiplied with the same exponential cutoff. The cutoff grows with applied force for materials spanning length scales from nanometers to kilometers. The tuneability of the cutoff with stress reflects "tuned critical" behavior, rather than self-organized criticality (SOC), which would imply stress-independence. A simple mean field model for avalanches of slipping weak spots explains the agreement across scales. It predicts the observed slip-size distributions and the observed stress-dependent cutoff function. The results enable extrapolations from one scale to another, and from one force to another, across different materials and structures, from nanocrystals to earthquakes.

Probing failure susceptibilities of earthquake faults using small-quake tidal correlations.

Mitigating the devastating economic and humanitarian impact of large earthquakes requires signals for forecasting seismic events. Daily tide stresses were previously thought to be insufficient for use as such a signal. Recently, however, they have been found to correlate significantly with small earthquakes, just before large earthquakes occur. Here we present a simple earthquake model to investigate whether correlations between daily tidal stresses and small earthquakes provide information about the likelihood of impending large earthquakes. The model predicts that intervals of significant correlations between small earthquakes and ongoing low-amplitude periodic stresses indicate increased fault susceptibility to large earthquake generation. The results agree with the recent observations of large earthquakes preceded by time periods of significant correlations between smaller events and daily tide stresses. We anticipate that incorporating experimentally determined parameters and fault-specific details into the model may provide new tools for extracting improved probabilities of impending large earthquakes.

Universal critical dynamics in high resolution neuronal avalanche data.

The tasks of neural computation are remarkably diverse. To function optimally, neuronal networks have been hypothesized to operate near a nonequilibrium critical point. However, experimental evidence for critical dynamics has been inconclusive. Here, we show that the dynamics of cultured cortical networks are critical. We analyze neuronal network data collected at the individual neuron level using the framework of nonequilibrium phase transitions. Among the most striking predictions confirmed is that the mean temporal profiles of avalanches of widely varying durations are quantitatively described by a single universal scaling function. We also show that the data have three additional features predicted by critical phenomena: approximate power law distributions of avalanche sizes and durations, samples in subcritical and supercritical phases, and scaling laws between anomalous exponents.

Tuning coupling: discrete changes in runaway avalanche sizes in disordered media.

Hysteretic systems may exhibit a runaway avalanche in which a large fraction of the constituents of the system collectively change state. It would be very valuable to understand the role that interaction strength between constituents plays in the size of such catastrophic runaway avalanches. We use a simple model, the random field Ising model, to study how the size of the runaway avalanche changes as the coupling between spins, J, is tuned. In particular, we calculate P(S), the distribution of size changes S in the runaway avalanche size as J comes close to a critical value J(c), and find that the distribution scales as P(S)∼S(-τ)D(S(σ)(J/J(c)-1)), with τ and σ critical exponents and D(x) a universal scaling function. In mean field theory we find τ=3/2, σ=1/2, and D(x)=exp[-(3x)(1/σ)/2]. On the basis of these results and previous studies, we also predict that for three dimensions τ=1.6 and σ=0.24.