Large coefficient of variation of inter-spike intervals induced by noise current in the resonate-and-fire model neuron.

Neuronal spike variability is a statistical property associated with the noise environment. Considering a linearised Hodgkin-Huxley model, we investigate how large spike variability can be induced in a typical stellate cell when submitted to constant and noise current amplitudes. For low noise current, we observe only periodic firing (active) or silence activities. For intermediate noise values, in addition to only active or inactive periods, we also identify a single transition from an initial spike-train (active) to silence dynamics over time, where the spike variability is low. However, for high noise current, we find intermittent active and silence periods with different values. The spike intervals during active and silent states follow the exponential distribution, which is similar to the Poisson process. For non-maximal noise current, we observe the highest values of inter-spike variability. Our results suggest sub-threshold oscillations as a possible mechanism for the appearance of high spike variability in a single neuron due to noise currents.

Recurrence quantification analysis for the identification of burst phase synchronisation.

In this work, we apply the spatial recurrence quantification analysis (RQA) to identify chaotic burst phase synchronisation in networks. We consider one neural network with small-world topology and another one composed of small-world subnetworks. The neuron dynamics is described by the Rulkov map, which is a two-dimensional map that has been used to model chaotic bursting neurons. We show that with the use of spatial RQA, it is possible to identify groups of synchronised neurons and determine their size. For the single network, we obtain an analytical expression for the spatial recurrence rate using a Gaussian approximation. In clustered networks, the spatial RQA allows the identification of phase synchronisation among neurons within and between the subnetworks. Our results imply that RQA can serve as a useful tool for studying phase synchronisation even in networks of networks.

Riddling: Chimera's dilemma.

We investigate the basin of attraction properties and its boundaries for chimera states in a circulant network of Hénon maps. It is known that coexisting basins of attraction lead to a hysteretic behaviour in the diagrams of the density of states as a function of a varying parameter. Chimera states, for which coherent and incoherent domains occur simultaneously, emerge as a consequence of the coexistence of basin of attractions for each state. Consequently, the distribution of chimera states can remain invariant by a parameter change, and it can also suffer subtle changes when one of the basins ceases to exist. A similar phenomenon is observed when perturbations are applied in the initial conditions. By means of the uncertainty exponent, we characterise the basin boundaries between the coherent and chimera states, and between the incoherent and chimera states. This way, we show that the density of chimera states can be not only moderately sensitive but also highly sensitive to initial conditions. This chimera's dilemma is a consequence of the fractal and riddled nature of the basin boundaries.

Synchronous behaviour in network model based on human cortico-cortical connections.

OBJECTIVE: We consider a network topology according to the cortico-cortical connection network of the human brain, where each cortical area is composed of a random network of adaptive exponential integrate-and-fire neurons. APPROACH: Depending on the parameters, this neuron model can exhibit spike or burst patterns. As a diagnostic tool to identify spike and burst patterns we utilise the coefficient of variation of the neuronal inter-spike interval. MAIN RESULTS: In our neuronal network, we verify the existence of spike and burst synchronisation in different cortical areas. SIGNIFICANCE: Our simulations show that the network arrangement, i.e. its rich-club organisation, plays an important role in the transition of the areas from desynchronous to synchronous behaviours.

Inference of topology and the nature of synapses, and the flow of information in neuronal networks.

The characterization of neuronal connectivity is one of the most important matters in neuroscience. In this work, we show that a recently proposed informational quantity, the causal mutual information, employed with an appropriate methodology, can be used not only to correctly infer the direction of the underlying physical synapses, but also to identify their excitatory or inhibitory nature, considering easy to handle and measure bivariate time series. The success of our approach relies on a surprising property found in neuronal networks by which nonadjacent neurons do "understand" each other (positive mutual information), however, this exchange of information is not capable of causing effect (zero transfer entropy). Remarkably, inhibitory connections, responsible for enhancing synchronization, transfer more information than excitatory connections, known to enhance entropy in the network. We also demonstrate that our methodology can be used to correctly infer directionality of synapses even in the presence of dynamic and observational Gaussian noise, and is also successful in providing the effective directionality of intermodular connectivity, when only mean fields can be measured.

Synchronised firing patterns in a random network of adaptive exponential integrate-and-fire neuron model.

We have studied neuronal synchronisation in a random network of adaptive exponential integrate-and-fire neurons. We study how spiking or bursting synchronous behaviour appears as a function of the coupling strength and the probability of connections, by constructing parameter spaces that identify these synchronous behaviours from measurements of the inter-spike interval and the calculation of the order parameter. Moreover, we verify the robustness of synchronisation by applying an external perturbation to each neuron. The simulations show that bursting synchronisation is more robust than spike synchronisation.

Spike timing-dependent plasticity induces non-trivial topology in the brain.

We study the capacity of Hodgkin-Huxley neuron in a network to change temporarily or permanently their connections and behavior, the so called spike timing-dependent plasticity (STDP), as a function of their synchronous behavior. We consider STDP of excitatory and inhibitory synapses driven by Hebbian rules. We show that the final state of networks evolved by a STDP depend on the initial network configuration. Specifically, an initial all-to-all topology evolves to a complex topology. Moreover, external perturbations can induce co-existence of clusters, those whose neurons are synchronous and those whose neurons are desynchronous. This work reveals that STDP based on Hebbian rules leads to a change in the direction of the synapses between high and low frequency neurons, and therefore, Hebbian learning can be explained in terms of preferential attachment between these two diverse communities of neurons, those with low-frequency spiking neurons, and those with higher-frequency spiking neurons.

Model for tumour growth with treatment by continuous and pulsed chemotherapy.

In this work we investigate a mathematical model describing tumour growth under a treatment by chemotherapy that incorporates time-delay related to the conversion from resting to hunting cells. We study the model using values for the parameters according to experimental results and vary some parameters relevant to the treatment of cancer. We find that our model exhibits a dynamical behaviour associated with the suppression of cancer cells, when either continuous or pulsed chemotherapy is applied according to clinical protocols, for a large range of relevant parameters. When the chemotherapy is successful, the predation coefficient of the chemotherapic agent acting on cancer cells varies with the infusion rate of chemotherapy according to an inverse relation. Finally, our model was able to reproduce the experimental results obtained by Michor and collaborators [Nature 435 (2005) 1267] about the exponential decline of cancer cells when patients are treated with the drug glivec.