Acute Lin et al., 2014; Hassinen et al.,

Acute temperature changes significantly change
the duration and shape of pacemaker, atrial and ventricular APs of fish hearts
by altering the flow of inward and outward currents via the SL in
temperature-dependent manner (Harper et al., 1995; Vornanen et al., 2002;
Haverinen and Vornanen, 2007; Haverinen and Vornanen, 2009; Ballesta et al.,
2012; Vornanen et al., 2014; Lin et al., 2014; Hassinen et al., 2014; Shiels et
al., 2015). APD must inversly correlate with fH to allow
sufficient time for systole and diastole durations, otherwise diastole will
disappear under high fH, i.e, increasing in temperature
increases fH and decreases APD. In exercise and active fishes
(as tunas) and tropical fishes (as zebrafish) have higher fH
and shorter APD in comparison with dormant fishes (as crucian carp) or fishes
live in cold polar waters (as navaga). The shape and duration of fish cardiac
APs and the underlying ion currents are highly sensitive to temperature changes
and crucial in thermal acclimation or acclimatization of both freshwater and
marine teleosts to seasonal temperature regimes (Haverinen and Vornanen, 2009;
Galli et al., 2009; Hassinen et al., 2014; Abramochkin and Vornanen, 2015;
Vornanen and Hassinen, 2016).

 

1.6.3  Effect of temperature on ion currents/channels

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The cardiac APs are triggered by a
harmonious co-operation between depolarization (inward) and repolarization
(outward) ion currents. Depolarization is mainly achieved by the inward flow of
Na+ and Ca2+ ions, while repolarization achieved mainly by
the outward flow of K+ ions (Hodgkin and Huxley, 1952; Opie, 1998;
Bers, 2001). Ion channels in cardiac myocytes of fishes should be flexible and strongly
respond to temperature changes (Haverinen and Vornanen, 2004; Hassinen et al.,
2007; Hassinen et al., 2008; Haverinen and Vornanen, 2009; Galli et al., 2009;
Abramochkin and Vornanen, 2015), thence they have a profound role in thermal
tolerance and temperature acclimation/acclimatization of cardiac function. Channel
composition and underline subunits are different between species-specific and
may set the upper thermal tolerance of electrical excitability in fish heart
and thereby the ability of fishes to accommodate to the predicted global
heating (Hassinen et al. 2007; Hassinen et al. 2008; Somero 2010; Hassinen et
al. 2014).

The density of
INa is the center factor in determining the rate of AP propagation
over the heart and activates other ion channels to produce chamber-specific AP.
(Fozzard and Hanck, 1996; Schram et al., 2002; Kleber and Rudy, 2004). Thermal acclimation
effect on INa density is variable between species which propably due
to differences in fishes activity of lifestyle. The density of INa
was larger in cold-active (rainbow trout) than cold-dormant (crucian carp)
fishes. INa is higher in cold-acclimated rainbow trout (4°C) than in warm acclimated fishes (18°C ).
Contrary, INa is higher in warm acclimated crucian carp than cold
acclimated fishes (Haverinen and Vornanen, 2004). Also, the molecular
composition shifts in temperature-dependent manner, where the predominance isoform
in cold-active rainbow trout is Nav1.4 that was higher in cold
acclimated (4°C) than warm acclimated (18°C) fishes, while Nav1.5
was the predominance in cold-dormant crucian carp with slightly equal expressed
in winter and summer acclimatized fishes (Haverinen and Vornanen 2007, Tikkanen
et al. 2017).

ICaL
is the primary path for the majority of Ca2+ influx for activation
of the myofilaments during EC coupling in most of fishes and maintains the long
plateau duration of the cardiac AP through the balance with outward K+
currents (Hove-Madsen and Tort, 1998; Vornanen, 1998). Decrease in temperature declines
the Ca2+ sensitivity of the myofilaments and declines the density of
ICa (Cavalié et al., 1985; Harrison and Bers, 1990). ICa
density increased with acute increasing in temperature in most of fish species
(Shiels et al., 2000; Shiels et al., 2006; Galli et al., 2011; Shiels and Galli,
2014; Vornanen et al., 2014; Kubly and Stecyk, 2015). Thermal acclimation has
no effect on the density of ICa in rainbow trout and crucian carp ventricular
myocytes when measured at room temperature (Vornanen, 1998). Contrary, seasonal
acclimatized has a striking effect on ICa density in ventricular
myocytes of crucian carp and the ICa density in summer acclimatized
carp was higher than that in winter acclimatized carp at 11°C (Vornanen and
Paajanen, 2004). The temperature sensitivity of ICa in fishes is
within the lower range of those found in most of mammals (Kim et al., 2000;
Shiels et al., 2000; Shiels et al., 2006).in contrast with INa, transcripts
of ICaL channels are slightly affected by seasons in ventricular
myocytes of crucian carp (Tiitu and Vornanen, 2003; Vornanen and Paajanen, 2004;
Tikkanen et al., 2017).

Fish
cardiomyocytes have two major K+ currents, the background inward
rectifier K+ current (IK1) and the rapid component of the
rapid delayed rectifier K+ current (IKr) (Vornanen et al.,
2002; Hassinen et al., 2007; Haverinen and Vornanen, 2009). IK1 is
responsible for maintaining the negative resting membrane potential RMP and set
the rate of AP repolarization (Vornanen et al., 2002), while IKr
modulates the AP duration (APD) (Haverinen and Vornanen, 2009). Acute changes
in temperature have strongly effect on the density of IK1 and IKr
in thermal acclimated and seasonal acclimatized fishes (Paajanen and
Vornanen, 2004; Haverinen and Vornanen, 2009; Galli et al., 2009; Abramochkin
and Vornanen, 2015). In the most of studied fishes, IKr is
upregulated by cold-acclimtion where the density of IKr is higher in
cold acclimated fishes than warm acclimated fishes (Haverinen and Vornanen,
2009; Galli et al., 2009; Hassinen et al., 2014; Abramochkin and Vornanen, 2015).
Moreover, there is a close correlation between the density of IKr and
fH in cold- and warm-acclimated fishes (Vornanen, 2016). Contrary,
temperature-dependent of IK1 density varies from species to other,
where IK1 density was higher in cold acclimated crucian carp, roach
and perch than warm acclimated fishes in atrial and ventricular myocytes, while
it was higher in warm acclimated perch than cold acclimated fish. Also, there are
differences between atrial and ventricular IK1 in the same fish, e.g.
IK1 density was higher in atrial myocytes of warm acclimated burbot
and Pacific bluefin tuna (Thunnus thynnus) than cold acclimated fishes,
while it was higher in ventricular myocytes of cold acclimated fishes than warm
acclimated (Haverinen and Vornanen, 2009; Galli et al.,  2009). In seasonal acclimatized navaga and
thermal acclimated roach, IK1 density in ventricular myocytes was
higher in warm- than cold-acclimated fishes (Haverinen and Vornanen, 2009; Abramochkin
and Vornanen, 2015).

Temperature-dependent
changes in K+ current density in fish cardiomyocytes are associated
with changes in gene expression either at the transcript or protein level. IK1
and IKr are produced by Kir2 and Erg isoforms channels,
respectively.

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