Why strengthening gap junctions may hinder action potential propagation

TL;DR

This paper presents a theoretical analysis of how gap junction conductance affects action potential propagation, revealing that both too weak or too strong conductance can hinder signal transmission and introducing the concept of semi-active propagation.

Contribution

It introduces a new theoretical model explaining the optimal gap junction conductance for action potential propagation and identifies semi-active propagation as a novel behavior.

Findings

Optimal gap junction conductance exists for reliable AP propagation

Both weaker and stronger conductance can block propagation

Semi-active propagation allows signal transmission without resting excitability

Abstract

Gap junctions are channels in cell membranes allowing ions to pass directly between cells. They connect cells throughout the body, including heart myocytes, neurons, and astrocytes. Propagation mediated by gap junctions can be passive or active. In passive propagation, the membrane potential of one cell influences that of neighboring cells without triggering action potentials (APs). In active propagation, an AP in one cell triggers APs in neighboring cells; this occurs in cardiac tissue and throughout the nervous system. It is known experimentally that there is an ideal gap junction conductance for AP propagation -- weaker or stronger conductance can block propagation. We present a theory explaining this phenomenon by analyzing an idealized model that focuses exclusively on gap junctional and spike-generating currents. We also find a novel type of behavior that we call semi-active propagation, in which cells in the network are not excitable at rest, but still propagate action potentials.