Computational modeling suggests that adaptive gap junctions may play a key role in cardiac memory and cellular synchronization.
May guide arrhythmia modeling but should not change practice; leaves open adaptive gap junctions' role in human cardiac memory.
Memory in the nervous system is essentially a network effect, resulting from synaptic adaptation in a network of neurons. The heart too is a network of cardiac cells electrically coupled by gap junctions, which, we hypothesize, adapt as a function of the state of cellular depolarization. Cardiac memory, which refers to persistent effect of external stimulus on activation pattern, is demonstrated in a pair of model Noble cells with adaptive gap junctions. The memory seems to have a dual effect: while it dissipates small perturbations, it captures and imprints larger ones. The proposed memory mechanism is also shown to increase likelihood of synchronization among cardiac cells. Finally we argue that the proposed mechanism is linked to known electrophysiological properties of gap junctions
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Krishnan et al. (2005) studied this question.
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