Modeling brain activation patterns for the default and cognitive states

Abstract

We argue that spatial patterns of cortical activation observed with EEG, MEG and fMRI might arise from spontaneous self-organisation of interacting populations of excitatory and inhibitory neurons. We examine the dynamical behavior of a mean-field cortical model that includes chemical and electrical (gap-junction) synapses, focusing on two limiting cases: the “slow-soma” limit with slow voltage feedback from soma to dendrite, and the “fast-soma” limit in which the feedback action of soma voltage onto dendrite reversal potentials is instantaneous. For slow soma-dendrite feedback, we find a low-frequency (∼1 Hz) dynamic Hopf instability, and a stationary Turing instability that catalyzes formation of patterned distributions of cortical firing-rate activity with pattern wavelength ∼2 cm. Turing instability can only be triggered when gap-junction diffusion between inhibitory neurons is strong, but patterning is destroyed if the tonic level of subcortical excitation is raised sufficiently. Interaction between the Hopf and Turing instabilities may describe the non-cognitive background or “default” state of the brain, as observed by BOLD imaging. In the fast-soma limit, the model predicts a high-frequency Hopf (∼35 Hz) instability, and a traveling-wave gamma-band instability that manifests as a 2-D standing-wave pattern oscillating in place at ∼30 Hz. Small levels of inhibitory diffusion enhance and broaden the definition of the gamma antinodal regions by suppressing higher-frequency spatial modes, but gamma emergence is not contingent on the presence of inhibitory gap junctions; higher levels of diffusion suppress gamma activity. Fast-soma instabilities are enhanced by increased subcortical stimulation. Prompt soma-dendrite feedback may be an essential component of the genesis and large-scale cortical synchrony of gamma activity observed at the point of cognition.