Nastaran Lotfi, Antonio J. Fontenele, Thaís Feliciano, Leandro A. A. Aguiar, Nivaldo A. P. de Vasconcelos, Carina Soares-Cunha, Bárbara Coimbra, Ana João Rodrigues, Nuno Sousa, Mauro Copelli, Pedro V. Carelli
It has recently been reported that statistical signatures of brain criticality, obtained from distributions of neuronal avalanches, can depend on the cortical state. We revisit these claims with a completely different and independent approach, employing a maximum entropy model to test whether signatures of criticality appear in urethane-anesthetized rats. To account for the spontaneous variation of cortical state, we parse the time series and perform the maximum entropy analysis as a function of the variability of the population spiking activity. To compare data sets with different number of neurons, we define a normalized distance to criticality that takes into account the peak and width of the specific heat curve. We found an universal collapse of the normalized distance to criticality dependence on the cortical state on an animal by animal basis. This indicates a universal dynamics and a critical point at an intermediate value of spiking variability.
Cecilia Romaro, Antonio Carlos Roque, Jose Roberto Castilho Piqueira
There is a strong nexus between the network size and the computational resources available, which may impede a neuroscience study. In the meantime, rescaling the network while maintaining its behavior is not a trivial mission. Additionally, modeling patterns of connections under topographic organization presents an extra challenge: to solve the network boundaries or mingled with an unwished behavior. This behavior, for example, could be an inset oscillation due to the torus solution; or a blend with/of unbalanced neurons due to a lack (or overdose) of connections. We detail the network rescaling method able to sustain behavior statistical utilized in Romaro et al. (2018) and present a boundary solution method based on the previous statistics recoup idea.
Iara Frondana, Rodrigo R.S. Carvalho, Florencia Leonardi
Epilepsy has been a central topic in computational neuroscience, and in silico models have shown to be excellent tools to integrate and evaluate findings from animal and clinical settings. Among the different languages and tools for computational modeling development, NEURON stands out as one of the most used and mature neurosimulators. However, despite the vast quantity of models developed with NEURON, a fragmentation problem is evident in the great majority of models related to the same type of cell or cell properties. This fragmentation causes a lack of interoperability between the models because of differences in parameters.
Cecilia Romaro, Fernando Araujo Najman, Morgan André
In this paper we present a numerical study of a mathematical model of spiking neurons introduced by Ferrari et al. in an article entitled Phase transition forinfinite systems of spiking neurons. In this model we have a countable number of neurons linked together in a network, each of them having a membrane potential taking value in the integers, and each of them spiking over time at a rate which depends on the membrane potential through some rate function ϕ. Beside being affected by a spike each neuron can also be affected by leaking. At each of these leak times, which occurs for a given neuron at a fixed rate γ, the membrane potential of the neuron concerned is spontaneously reset to 0.
Antonio Galves, Eva Löcherbach, Christophe Pouzat, Errico Presutti
In this paper we present a simple microscopic stochastic model describing short term plasticity within a large homogeneous network of interacting neurons. Each neuron is represented by its membrane potential and by the residual calcium concentration within the cell at a given time. Neurons spike at a rate depending on their membrane potential. When spiking, the residual calcium concentration of the spiking neuron increases by one unit. Moreover, an additional amount of potential is given to all other neurons in the system. This amount depends linearly on the current residual calcium concentration within the cell of the spiking neuron. In between successive spikes, the potentials and the residual calcium concentrations of each neuron decrease at a constant rate.
