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

Acknowledgements This study was possible by partial financial support from the following Brazilian government agencies: CNPq, CAPES, and FAPESP (2011/19296-1 and 2015/07311-7). We also wish thank Newton Fund and COFAP.Peer reviewedPostprin

Bistable Firing Pattern in a Neural Network Model

Excessively high, neural synchronization has been associated with epileptic seizures, one of the most common brain diseases worldwide. A better understanding of neural synchronization mechanisms can thus help control or even treat epilepsy. In this paper, we study neural synchronization in a random network where nodes are neurons with excitatory and inhibitory synapses, and neural activity for each node is provided by the adaptive exponential integrate-and-fire model. In this framework, we verify that the decrease in the influence of inhibition can generate synchronization originating from a pattern of desynchronized spikes. The transition from desynchronous spikes to synchronous bursts of activity, induced by varying the synaptic coupling, emerges in a hysteresis loop due to bistability where abnormal (excessively high synchronous) regimes exist. We verify that, for parameters in the bistability regime, a square current pulse can trigger excessively high (abnormal) synchronization, a process that can reproduce features of epileptic seizures. Then, we show that it is possible to suppress such abnormal synchronization by applying a small-amplitude external current on > 10% of the neurons in the network. Our results demonstrate that external electrical stimulation not only can trigger synchronous behavior, but more importantly, it can be used as a means to reduce abnormal synchronization and thus, control or treat effectively epileptic seizures.Peer Reviewe

Bistable firing pattern in a neural network model

Excessively high, neural synchronization has been associated with epileptic seizures, one of the most common brain diseases worldwide. A better understanding of neural synchronization mechanisms can thus help control or even treat epilepsy. In this paper, we study neural synchronization in a random network where nodes are neurons with excitatory and inhibitory synapses, and neural activity for each node is provided by the adaptive exponential integrate-and-fire model. In this framework, we verify that the decrease in the influence of inhibition can generate synchronization originating from a pattern of desynchronized spikes. The transition from desynchronous spikes to synchronous bursts of activity, induced by varying the synaptic coupling, emerges in a hysteresis loop due to bistability where abnormal (excessively high synchronous) regimes exist. We verify that, for parameters in the bistability regime, a square current pulse can trigger excessively high (abnormal) synchronization, a process that can reproduce features of epileptic seizures. Then, we show that it is possible to suppress such abnormal synchronization by applying a small-amplitude external current on > 10% of the neurons in the network. Our results demonstrate that external electrical stimulation not only can trigger synchronous behavior, but more importantly, it can be used as a means to reduce abnormal synchronization and thus, control or treat effectively epileptic seizures. © 2019 Protachevicz, Borges, Lameu, Ji, Iarosz, Kihara, Caldas, Szezech, Baptista, Macau, Antonopoulos, Batista and Kurths

Influence of Delayed Conductance on Neuronal Synchronization

In the brain, the excitation-inhibition balance prevents abnormal synchronous behavior. However, known synaptic conductance intensity can be insufficient to account for the undesired synchronization. Due to this fact, we consider time delay in excitatory and inhibitory conductances and study its effect on the neuronal synchronization. In this work, we build a neuronal network composed of adaptive integrate-and-fire neurons coupled by means of delayed conductances. We observe that the time delay in the excitatory and inhibitory conductivities can alter both the state of the collective behavior (synchronous or desynchronous) and its type (spike or burst). For the weak coupling regime, we find that synchronization appears associated with neurons behaving with extremes highest and lowest mean firing frequency, in contrast to when desynchronization is present when neurons do not exhibit extreme values for the firing frequency. Synchronization can also be characterized by neurons presenting either the highest or the lowest levels in the mean synaptic current. For the strong coupling, synchronous burst activities can occur for delays in the inhibitory conductivity. For approximately equal-length delays in the excitatory and inhibitory conductances, desynchronous spikes activities are identified for both weak and strong coupling regimes. Therefore, our results show that not only the conductance intensity, but also short delays in the inhibitory conductance are relevant to avoid abnormal neuronal synchronization.Peer Reviewe

Influence of Autapses on Synchronization in Neural Networks With Chemical Synapses

A great deal of research has been devoted on the investigation of neural dynamics in various network topologies. However, only a few studies have focused on the influence of autapses, synapses from a neuron onto itself via closed loops, on neural synchronization. Here, we build a random network with adaptive exponential integrate-and-fire neurons coupled with chemical synapses, equipped with autapses, to study the effect of the latter on synchronous behavior. We consider time delay in the conductance of the pre-synaptic neuron for excitatory and inhibitory connections. Interestingly, in neural networks consisting of both excitatory and inhibitory neurons, we uncover that synchronous behavior depends on their synapse type. Our results provide evidence on the synchronous and desynchronous activities that emerge in random neural networks with chemical, inhibitory and excitatory synapses where neurons are equipped with autapses. © Copyright © 2020 Protachevicz, Iarosz, Caldas, Antonopoulos, Batista and Kurths

Mathematical modelling and brain dynamical networks

In this thesis, we study the dynamics of the Hindmarsh-Rose (HR) model which studies the spike-bursting behaviour of the membrane potential of a single neuron. We study the stability of the HR system and compute its Lyapunov exponents (LEs). We consider coupled general sections of the HR system to create an undirected brain dynamical network (BDN) of Nn neurons. Then, we study the concepts of upper bound of mutual information rate (MIR) and synchronisation measure and their dependence on the values of electrical and chemical couplings. We analyse the dynamics of neurons in various regions of parameter space plots for two elementary examples of 3 neurons with two different types of electrical and chemical couplings. We plot the upper bound Ic and the order parameter rho (the measure of synchronisation) and the two largest Lyapunov exponents LE1 and LE2 versus the chemical coupling gn and electrical coupling gl. We show that, even for small number of neurons, the dynamics of the system depends on the number of neurons and the type of coupling strength between them. Finally, we evolve a network of Hindmarsh-Rose neurons by increasing the entropy of the system. In particular, we choose the Kolmogorov-Sinai entropy: HKS (Pesin identity) as the evolution rule. First, we compute the HKS for a network of 4 HR neurons connected simultaneously by two undirected electrical and two undirected chemical links. We get different entropies with the use of different values for both the chemical and electrical couplings. If the entropy of the system is positive, the dynamics of the system is chaotic and if it is close to zero, the trajectory of the system converges to one of the fixed points and loses energy. Then, we evolve a network of 6 clusters of 10 neurons each. Neurons in each cluster are connected only by electrical links and their connections form small-world networks. The six clusters connect to each other only by chemical links. We compare between the combined effect of chemical and electrical couplings with the two concepts, the information flow capacity Ic and HKS in evolving the BDNs and show results that the brain networks might evolve based on the principle of the maximisation of their entropies

The Effect of Input from the Cerebellar Nuclei on Activity in Thalamocortical Networks

The cerebellum is a prominent brain structure that contains more than half of all neurons, in the brain, which are densely packed and make up 15% of the total brain mass (Andersen et al., 1992). It is well known for its contribution to the control of motor functions, but it also plays a pivotal role in non-motor behaviours. The cerebellum is also involved in numerous pathological conditions. This thesis contributes to the understanding of the pathophysiology of the cerebello-thalamo-cortical pathways. I concentrate on two cerebellar diseases, namely: absence epilepsy (Noebels, 2005) and downbeat nystagmus (DBN) (Strupp et al., 2007). In this thesis the missing link in explaining the alleviating mechanism of a potassium channel blocker on downbeat nystagmus was found. A simulated single biologically detailed floccular target neuron (FTN) model was stimulated by input from cerebellar Purkinje cells (PCs). It was demonstrated that for both synchronised and unsynchronised input, irregular PC spike trains (which resembles the DBN condition) resulted in elevated FTN firing rates, in comparison with regular (4-AP treated) ones. This increase or decrease of the FTN firing rates during DBN, or after 4-AP treatment, respectively depended on short term depression (STD) at the PC - FTN synapses exclusively in the cases when the PC input was unsynchronised. In contrast, results of previous modelling studies (Glasauer et al, 2011; Glasauer and Rossert, 2008) were not in-line with the corresponding experimental findings (Alvina and Khodakhah, 2010) because they did not take into account the STD on the FTN-PC synapses. It was also demonstrated here that the cerebellar output contributes to the control of absence epilepsy that originates in the thalamocortical network. Moreover, the cerebellar input was most effective when it arrived at the peak of the GSWD burst, with the least effective input arriving during the inter-ictal interval, showing clear phase-dependency. I have also shown that a three-fold increase in the inhibitory time constant, drives the asynchronous-irregular network into an ictal state. This increase reflects the GABAA block. A change to GABAB dominated inhibition results in GSWDs, in which the “wave” component is related to the slow GABAB-mediated K+ currents (Destexhe, 1998). Therefore, in this thesis two important contributions are made to the understanding of cerebellar pathological states: absence epilepsy and DBN, which might in turn be useful in the potential treatment of these conditions.