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A Simple Stimulatory Device for Evoking Point-like Tactile Stimuli: A Searchlight for LFP to Spike Transitions
Published on: March 25, 2014
Population spiking and bursting in next-generation neural masses with spike-frequency adaptation
Alberto Ferrara1, David Angulo-Garcia2, Alessandro Torcini3,4,5
1Sorbonne Université, INSERM, CNRS, Institut de la Vision, 75012 Paris, France.
Abstract:
Spike-frequency adaptation (SFA) is a fundamental neuronal mechanism taking into account the fatigue due to spike emissions and the consequent reduction of the firing activity. We have studied the effect of this adaptation mechanism on the macroscopic dynamics of excitatory and inhibitory networks of quadratic integrate-and-fire (QIF) neurons coupled via exponentially decaying post-synaptic potentials. In particular, we have studied the population activities by employing an exact mean-field reduction, which gives rise to next-generation neural mass models. This low-dimensional reduction allows for the derivation of bifurcation diagrams and the identification of the possible macroscopic regimes emerging both in a single and in two identically coupled neural masses. In single populations SFA favors the emergence of population bursts in excitatory networks, while it hinders tonic population spiking for inhibitory ones. The symmetric coupling of two neural masses, in absence of adaptation, leads to the emergence of macroscopic solutions with broken symmetry, namely, chimera-like solutions in the inhibitory case and antiphase population spikes in the excitatory one. The addition of SFA leads to new collective dynamical regimes exhibiting cross-frequency coupling (CFC) among the fast synaptic timescale and the slow adaptation one, ranging from antiphase slow-fast nested oscillations to symmetric and asymmetric bursting phenomena. The analysis of these CFC rhythms in the θ-γ range has revealed that a reduction of SFA leads to an increase of the θ frequency joined to a decrease of the γ one. This is analogous to what has been reported experimentally for the hippocampus and the olfactory cortex of rodents under cholinergic modulation, which is known to reduce SFA.
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