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Spiral waves are spatial-temporal patterns that can emerge in different systems as heart tissues, chemical oscillators, ecological networks and the brain. These waves have been identified in the neocortex of turtles, rats, and humans, particularly during sleep-like states. Although their functions in cognitive activities remain until now poorly understood, these patterns are related to cortical activity modulation and contribute to cortical processing. In this work, we construct a neuronal network layer based on the spatial distribution of pyramidal neurons. Our main goal is to investigate how local connectivity and coupling strength are associated with the emergence of spiral waves. Therefore, we propose a trustworthy method capable of detecting different wave patterns, based on local and global phase order parameters. As a result, we find that the range of connection radius (R) plays a crucial role in the appearance of spiral waves. For R < 20 {\mu}m, only asynchronous activity is observed due to small number of connections. The coupling strength (gsyn ) greatly influences the pattern transitions for higher R, where spikes and bursts firing patterns can be observed in spiral and non-spiral waves. Finally, we show that for some values of R and gsyn bistable states of wave patterns are obtained.

We study the time delay in the synaptic conductance for suppression of spike synchronisation in a random network of Hodgkin Huxley neurons coupled by means of chemical synapses. In the first part, we examine in detail how the time delay acts over the network during the synchronised and desynchronised neuronal activities. We observe a relation between the neuronal dynamics and the syaptic conductance distributions. We find parameter values in which the time delay has high effectiveness in promoting the suppression of spike synchronisation. In the second part, we analyse how the delayed neuronal networks react when pulsed inputs with different profiles (periodic, random, and mixed) are applied on the neurons. We show the main parameters responsible for inducing or not synchronous neuronal oscillations in delayed networks.

The brain has the phenomenal ability to reorganize itself by forming new connections among neurons and by pruning others. The so-called neural or brain plasticity facilitates the modification of brain structure and function over different time scales. Plasticity might occur due to external stimuli received from the environment, during recovery from brain injury, or due to modifications within the body and brain itself. In this paper, we study the combined effect of short-term (STP) and spike-timing-dependent plasticities (STDP) on the synaptic strength of excitatory coupled Hodgkin-Huxley neurons and show that plasticity can facilitate the formation of modular neural networks with complex topologies that resemble those of networks with preferential attachment properties. In particular, we use an STDP rule that alters the synaptic coupling intensity based on time intervals between spikes of postsynaptic and presynaptic neurons. Previous works have shown that STDP may induce the appearance of directed connections from high to low-frequency spiking neurons. On the other hand, STP is attributed to the release of neurotransmitters in the synaptic cleft of neurons that alter its synaptic efficiency. Our results suggest that the combined effect of STP and STDP with high recovery time facilitates the formation of connections among neurons with similar spike frequencies only, a kind of preferential attachment. We then pursue this further and show that, when starting with all-to-all neural configurations, depending on the STP recovery time and distribution of neural frequencies, modular neural networks can emerge as a direct result of the combined effect of STP and STDP., Comment: 18 pages, 11 figures

Small-world structures are often used to describe structural connections in the brain. In this work, we compare the structural connection of cortical areas of a healthy brain and a brain affected by Alzheimer's disease with artificial small-world networks. Based on statistics analysis, we demonstrate that similar small-world networks can be constructed using Newman-Watts procedure. The network quantifiers of both structural matrices are identified inside the probabilistic valley. Despite of similarities between structural connection matrices and sampled small-world networks, increased assortativity can be found in the Alzheimer brain. Our results indicate that network quantifiers can be helpful to identify abnormalities in real structural connection matrices.

Chimera states are spatiotemporal patterns in which coherence and incoherence coexist. We observe the coexistence of synchronous (coherent) and desynchronous (incoherent) domains in a neuronal network. The network is composed of coupled adaptive exponential integrate-and-fire neurons that are connected by means of chemical synapses. In our neuronal network, the chimera states exhibit spatial structures both with spikes and bursts activities. Furthermore, those desynchronised domains not only have either spike or burst activity, but we show that the structures switch between spikes and bursts as the time evolves. Moreover, we verify the existence of multicluster chimera states.

Brain plasticity, also known as neuroplasticity, is a fundamental mechanism of neuronal adaptation in response to changes in the environment or due to brain injury. In this review, we show our results about the effects of synaptic plasticity on neuronal networks composed by Hodgkin-Huxley neurons. We show that the final topology of the evolved network depends crucially on the ratio between the strengths of the inhibitory and excitatory synapses. Excitation of the same order of inhibition revels an evolved network that presents the rich-club phenomenon, well known to exist in the brain. For initial networks with considerably larger inhibitory strengths, we observe the emergence of a complex evolved topology, where neurons sparsely connected to other neurons, also a typical topology of the brain. The presence of noise enhances the strength of both types of synapses, but if the initial network has synapses of both natures with similar strengths. Finally, we show how the synchronous behaviour of the evolved network will reflect its evolved topology.

We have studied effects of perturbations on the cat cerebral cortex. According to the literature, this cortex structure can be described by a clustered network. This way, we construct a clustered network with the same number of areas as in the cat matrix, where each area is described as a sub-network with small-world property. We focus on the suppression of neuronal phase synchronisation considering different kinds of perturbations. Among the various controlling interventions, we choose three methods: delayed feedback control, external time-periodic driving, and activation of selected neurons. We simulate these interventions to provide a procedure to suppress undesired and pathological abnormal rhythms that can be associated with many forms of synchronisation. In our simulations, we have verified that the efficiency of synchronisation suppression by delayed feedback control is higher than external time-periodic driving and activation of selected neurons for the cat cerebral cortex with the same coupling strengths.

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 envolves 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., Comment: 8 pages, 6 figures