Abstract
Cardiac physiology of fish models is an emerging field given the ease of genome editing and the development of transgenic models. Several studies have described the cardiac properties of zebrafish (Denio rerio). The goldfish (Carassius auratus) belongs to the same family as the zebrafish and has emerged as an alternative model with which to study cardiac function. Here, we propose to acutely study electrophysiological and systolic Ca(2+) signaling in intact goldfish hearts. We assessed the Ca(2+) dynamics and the electrophysiological cardiac function of goldfish, zebrafish, and mice models, using pulsed local field fluorescence microscopy, intracellular microelectrodes, and flash photolysis in perfused hearts. We observed goldfish ventricular action potentials (APs) and Ca(2+) transients to be significantly longer when compared to the zebrafish. The action potential half duration at 50% (APD(50)) of goldfish was 370.38 ± 8.8 ms long, and in the zebrafish they were observed to be only 83.9 ± 9.4 ms. Additionally, the half duration of the Ca(2+) transients was also longer for goldfish (402.1 ± 4.4 ms) compared to the zebrafish (99.1 ± 2.7 ms). Also, blocking of the L-type Ca(2+) channels with nifedipine revealed this current has a major role in defining the amplitude and the duration of goldfish Ca(2+) transients. Interestingly, nifedipine flash photolysis experiments in the intact heart identified whether or not the decrease in the amplitude of Ca(2+) transients was due to shorter APs. Moreover, an increase in temperature and heart rate had a strong shortening effect on the AP and Ca(2+) transients of goldfish hearts. Furthermore, ryanodine (Ry) and thapsigargin (Tg) significantly reduced the amplitude of the Ca(2+) transients, induced a prolongation in the APs, and altogether exhibited the degree to which the Ca(2+) release from the sarcoplasmic reticulum contributed to the Ca(2+) transients. We conclude that the electrophysiological properties and Ca(2+) signaling in intact goldfish hearts strongly resembles the endocardial layer of larger mammals.