Activity-Dependent Plasticity In Gap Junctions as a Mechanism for Cardiac Memory

Studies on the effects of external pacing of heart suggest that the organ, like the nervous system, possesses properties of memory and adaptation. Changes induced in cardiac activation patterns persist long after the agent that induced those changes is removed. After the effects of stimulation have disappeared, response to the stimulus applied for a second time is much greater than the earlier response. Drawing analogies between communication via gap junctions in cardiac tissue, and via synapses in nervous tissue, we hypothesize that gap junctions also adapt in an activity-dependent manner similar to synapses. With the help of a mathematical model of cardiac cell, the well-known FitzHugh-Nagumo model, we demonstrate that some of the clinically observed manifestations of cardiac memory property can be simulated if gap-junctional conductances are allowed to adapt according to a Hebb-like learning mechanism, a mechanism that successfully accounts for a range of learning and memory phenomena in nervous system.