I’m a PhD student in the lab of Dr. Steve Poelzing at FBRI, a research institute of Virginia Tech. We study cardiac electrophysiology (i.e. how electricity moves through the heart) in order to help develop novel diagnostics and therapies for arrhythmias. Our work often centers around the concept of ephaptic coupling, which is a theory of electrical conduction that is dependent on the very narrow spaces that exist between heart cells.

In the last few years, we’ve discovered that these narrow spaces, which were discovered by Dr. Rob Gourdie and dubbed the “perinexus”,  house large quantities of voltage gated sodium channels. This makes them excellent conductors of electricity from one cell to another.

For a more technical explanation: ). The theory of EpC posits that the activation of a sodium current on one side of a small intercellular cleft (such as the intercalated disc nanodomain known as the perinexus) results in a more negative extracellular potential and depolarizes the abutting cell, thereby activating its sodium channels and leading to conduction of the action potential (graphical depiction seen in figure 1). Accordingly, narrowing junctional extracellular spaces can theoretically result in faster membrane potential changes and increase CV.

Our lab has a few tools with which we can modify ephaptic coupling in isolated hearts from animal models of various diseases. Right now, my work is focused on modifying ephaptic coupling in a model of Brugada Syndrome. This is a rare genetic condition that can have severe consequences, like arrhythmia or sudden cardiac death in relatively young patients with no apparent heart disease. Hopefully, my work with ephaptic coupling modifications in mouse models can eventually lead to new therapies for this disease.