Abstract
SummaryCardiac stimulation via sympathetic neurons can potentially trigger arrhythmias. We present approaches to study neuron-cardiomyocyte interactions involving optogenetic selective probing and all-optical electrophysiology to measure activity in an automated fashion. Here we demonstrate the utility of optical interrogation of sympathetic neurons and their effects on macroscopic cardiomyocyte network dynamics to address research targets such as the effects of adrenergic stimulation via the release of neurotransmitters, the effect of neuronal numbers on cardiac behavior, and the applicability of optogenetics in mechanistic in vitro studies. As arrhythmias are emergent behaviors that involve the coordinated activity of millions of cells, we image at macroscopic scales to capture complex dynamics. We show that neurons can both decrease and increase wave stability and re-entrant activity in culture depending on their induced activity—a finding that may help us understand the often conflicting results seen in experimental and clinical studies.
Highlights
Cardiac impulse formation and conduction are modulated by autonomic activity, and the autonomic nervous system plays an important role in the initiation and maintenance of arrhythmias in diseased hearts (Bub and Burton, 2014; Herring et al, 2019; Winfree, 1987)
We present approaches to study neuron-cardiomyocyte interactions involving optogenetic selective probing and all-optical electrophysiology to measure activity in an automated fashion
We demonstrate the utility of optical interrogation of sympathetic neurons and their effects on macroscopic cardiomyocyte network dynamics to address research targets such as the effects of adrenergic stimulation via the release of neurotransmitters, the effect of neuronal numbers on cardiac behavior, and the applicability of optogenetics in mechanistic in vitro studies
Summary
Cardiac impulse formation and conduction are modulated by autonomic activity, and the autonomic nervous system plays an important role in the initiation and maintenance of arrhythmias in diseased hearts (Bub and Burton, 2014; Herring et al, 2019; Winfree, 1987). Tissue damage can alter the distribution of innervation where cardiac cell death following myocardial infarction causes sympathetic denervation followed by nerve sprouting and reinnervation (Gardner et al, 2016). Resolving the unclear pro- or antiarrhythmic effect of post-infarction reinnervation may involve the precise understanding of neural heterogeneity and its role in arrhythmia modulation. Research on these questions may benefit from the use of a cell culture model system where the effects of innervation can be precisely controlled.
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