Gap junction plasticity as a mechanism to regulate network-wide oscillations

TL;DR

This paper proposes a computational model demonstrating that activity-dependent gap junction plasticity in cortical interneurons acts as a homeostatic mechanism to regulate network oscillations, supporting robust neuronal communication.

Contribution

It introduces a novel computational model showing how gap junction plasticity can dynamically regulate cortical oscillations and facilitate information transmission.

Findings

Gap junction plasticity maintains balance between asynchronous and oscillatory states.

Plasticity enables transient oscillations and frequency modulation for communication.

Model suggests a functional role for gap junctions in cortical information processing.

Abstract

Cortical oscillations are thought to be involved in many cognitive functions and processes. Several mechanisms have been proposed to regulate oscillations. One prominent but understudied mechanism is gap-junctional coupling. Gap junctions are ubiquitous in cortex between GABAergic interneurons. Moreover, recent experiments indicate their strength can be modified in an activity-dependent manner, similar to chemical synapses. We hypothesized that activity-dependent gap junction plasticity acts as a mechanism to regulate oscillations in the cortex. We developed a computational model of gap junction plasticity in a recurrent cortical network. We showed that gap junction plasticity can serve as a homeostatic mechanism for oscillations by maintaining a tight balance between two network states: asynchronous irregular activity and synchronized oscillations. This homeostatic mechanism allows for robust communication between neuronal assemblies through two different mechanisms: transient oscillations and frequency modulation. This implies a direct functional role for gap junction plasticity in information transmission in cortex.