An organizing center in a planar model of neuronal excitability

The paper studies the excitability properties of a generalized FitzHugh-Nagumo model. The model differs from the purely competitive FitzHugh-Nagumo model in that it accounts for the effect of cooperative gating variables such as activation of calcium currents. Excitability is explored by unfolding a pitchfork bifurcation that is shown to organize five different types of excitability. In addition to the three classical types of neuronal excitability, two novel types are described and distinctly associated to the presence of cooperative variables

Minimum Number of Probes for Brain Dynamics Observability

In this paper, we address the problem of placing sensor probes in the brain such that the system dynamics' are generically observable. The system dynamics whose states can encode for instance the fire-rating of the neurons or their ensemble following a neural-topological (structural) approach, and the sensors are assumed to be dedicated, i.e., can only measure a state at each time. Even though the mathematical description of brain dynamics is (yet) to be discovered, we build on its observed fractal characteristics and assume that the model of the brain activity satisfies fractional-order dynamics. Although the sensor placement explored in this paper is particularly considering the observability of brain dynamics, the proposed methodology applies to any fractional-order linear system. Thus, the main contribution of this paper is to show how to place the minimum number of dedicated sensors, i.e., sensors measuring only a state variable, to ensure generic observability in discrete-time fractional-order systems for a specified finite interval of time. Finally, an illustrative example of the main results is provided using electroencephalogram (EEG) data.Comment: arXiv admin note: text overlap with arXiv:1507.0720

Ion channel degeneracy enables robust and tunable neuronal firing rates.

Firing rate is an important means of encoding information in the nervous system. To reliably encode a wide range of signals, neurons need to achieve a broad range of firing frequencies and to move smoothly between low and high firing rates. This can be achieved with specific ionic currents, such as A-type potassium currents, which can linearize the frequency-input current curve. By applying recently developed mathematical tools to a number of biophysical neuron models, we show how currents that are classically thought to permit low firing rates can paradoxically cause a jump to a high minimum firing rate when expressed at higher levels. Consequently, achieving and maintaining a low firing rate is surprisingly difficult and fragile in a biological context. This difficulty can be overcome via interactions between multiple currents, implying a need for ion channel degeneracy in the tuning of neuronal properties.This is the author accepted manuscript. The final version is available from National Academy of Sciences via http://dx.doi.org/10.1073/pnas.1516400112

Cell types, network homeostasis, and pathological compensation from a biologically plausible ion channel expression model.

How do neurons develop, control, and maintain their electrical signaling properties in spite of ongoing protein turnover and perturbations to activity? From generic assumptions about the molecular biology underlying channel expression, we derive a simple model and show how it encodes an "activity set point" in single neurons. The model generates diverse self-regulating cell types and relates correlations in conductance expression observed in vivo to underlying channel expression rates. Synaptic as well as intrinsic conductances can be regulated to make a self-assembling central pattern generator network; thus, network-level homeostasis can emerge from cell-autonomous regulation rules. Finally, we demonstrate that the outcome of homeostatic regulation depends on the complement of ion channels expressed in cells: in some cases, loss of specific ion channels can be compensated; in others, the homeostatic mechanism itself causes pathological loss of function.Charles A. King TrustThis is the final version of the article. It first appeared from Cell Press (Elsevier) via http://dx.doi.org/10.1016/j.neuron.2014.04.002

The geometry of rest–spike bistability

Funder: Qualcomm; doi: http://dx.doi.org/10.13039/100005144Abstract: Morris–Lecar model is arguably the simplest dynamical model that retains both the slow–fast geometry of excitable phase portraits and the physiological interpretation of a conductance-based model. We augment this model with one slow inward current to capture the additional property of bistability between a resting state and a spiking limit cycle for a range of input current. The resulting dynamical system is a core structure for many dynamical phenomena such as slow spiking and bursting. We show how the proposed model combines physiological interpretation and mathematical tractability and we discuss the benefits of the proposed approach with respect to alternative models in the literature