The role of inhibitory neuronal variability in modulating phase diversity between coupled networks

TL;DR

This paper investigates how inhibitory neuronal variability influences phase diversity and synchronization regimes between coupled cortical networks, revealing mechanisms for zero-lag synchronization and bistability relevant to brain communication.

Contribution

It demonstrates that inhibitory heterogeneity can induce phase diversity, anticipated synchronization, and bistability, providing new insights into neuronal communication mechanisms.

Findings

Heterogeneity enlarges zero-lag synchronization regions

Both homogeneous and heterogeneous networks show phase diversity

Heterogeneity modulates the transition from delayed to anticipated synchronization

Abstract

Neuronal heterogeneity, characterized by the presence of a multitude of spiking neuronal patterns, is a widespread phenomenon throughout the nervous system. In particular, the brain exhibits strong variability among inhibitory neurons. Despite the huge neuronal heterogeneity across brain regions, which in principle could decrease synchronization, cortical areas coherently oscillate during various cognitive tasks. Therefore, the functional significance of neuronal heterogeneity remains a subject of active investigation. Previous studies typically focus on the role of heterogeneity in the dynamic properties of only one population. Here, we explore how different types of inhibitory neurons can contribute to the diversity of the phase relations between two cortical areas. This research sheds light on the potential impact of local properties, such as neuronal variability, on communication between distant brain regions. We show that both homogeneous and heterogeneous inhibitory networks can exhibit phase diversity and nonintuitive regimes such as anticipated synchronization (AS) and phase bistability. It has been proposed that the bi-stable phase could be related to bi-stable perception, such as in the Necker cube. Moreover, we show that heterogeneity enlarges the region of zero-lag synchronization and bistability. We also show that the parameter controlling inhibitory heterogeneity modulates the transition from the usual delayed synchronization regime (DS) to AS. Finally, we show that the inhibitory heterogeneity drives the internal dynamics of the free-running population. Therefore, we suggest a possible mechanism to explain when the DS-AS transition occurs via zero-lag synchronization or bi-stability.