Is there something fishy about the regulation of the ryanodine receptor in the fish heart?

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The fish cardiac sarcoplasmic reticulum (SR) holds large quantities of Ca2+, but calcium-induced calcium release (CICR) is weak in these myocytes, and contraction and relaxation are largely determined by transsarcolemmal Ca2+ flux. Many fish species live in a cold and seasonally variable thermal habitat, which could provide challenges to regulation of excitation–contraction coupling. Here, we focus on the cardiac SR Ca2+-release channel (RyR2) in fish and ask whether it may be regulated in a different manner from the mammalian RyR2. We review data indicating that fish cardiac RyR are present at lower density, are more spatially separated within the SR membrane and are less responsive to cytosolic Ca2+ than mammalian RyR2 channels. All of these features would contribute to the weak CICR evident from functional studies. We also consider how CICR can be enhanced in fish myocytes following β-adrenergic stimulation and application of low levels of caffeine, and how acute and chronic temperature change may affect the gating properties of fish RyR2s. It is clear that a lack of insight into the fundamental gating and conductance properties of fish RyR2 channels is hindering our understanding of the role of the SR in fish cardiac excitation–contraction coupling. We conclude by reflecting on how studies that probe the biophysical properties of fish RyR2 channel gating in response to various ligands and temperatures would be very instructive for our understanding of the role of the SR in the evolution of the heart.

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