Voltage AP over the cardiac SL; and

Voltage gated Na+ channels are
consist of the pore-forming ?-subunits and auxillary ?-subunits (Catterall and
Waxman, 2005). The ?-subunit composed of four homologous domains (I-IV), each domain
has six transmembrane spans (S1-S6) with a pore (or P)
loop between S5 and S6 which may act to line the actual
permeation pore and involved in channel selectivity. The S4 span in
each domain is positively charged and coordinate the opening of the Na+ channel
in a voltage-dependent manner. The plug, the short intracellular loop
connecting domains III and IV, closes the channel upon inactivation (Catterall,
1992; Bers, 2001).

The opening of
Na+ channel causes the fast inward Na+ current (INa).
 INa is the first activated
current in the excitation of atrial and ventcular myocytes (AP: phase 0),
produces the fast AP upstroke and  AP
overshoot (Fozzard and Hanck, 1996). The density of INa determines
the rate of AP upstroke and the propagation velocity of the AP over the cardiac
SL; and provides the necessary charge to depolarize the cell membrane and
activate other ion channels in production of AP (Kleber and Rudy 2004, Schram
et al. 2002). K+ currents which responsible for maintaining the RMP
of AP have an indirect effect on INa by regulation the number of
available Na+ channels. The availability of Na+ channels
is dependent on the RMP, where the more negative RMP increases the avaliability
of Na+ channels and vise versa (Golod et al. 1998; Maltsev and
Undrovinas, 1998). In rainbow trout (Oncorhynchus mykiss) and zebrafish
(Danio rerio), INa density was similar in atrial and
ventricular myocytes. However, the voltage dependence of steady-state activation and inactivation for
trout and steady-state inactivation for zebrafish were more negative in atrial
than ventricular myocytes (Warren et al., 2001; Haverinen and Vornanen,
2006). The relatively negative voltage dependence of INa activation
together with the small size of inward rectifier K+ current (IK1)
make atrial myocytes easily excitable by the depolarization wav from the
pacemaker cells.

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Fish have eight
genes encode ?-subunits of the voltage-gated Na+ channels, while
mammals have nine Na+ channel genes. In mammalian hearts, INa
is mainly produced by Nav1.5 ?-subunits, while in rainbow trout the
main cardiac isoform is Nav1.4 and only small amounts of Nav1.5
and Nav1.6 are expressed. In crucian carp (Carassius carassius)
and zebrafish, Nav1.5 is the main cardiac isoform, although they
express some Nav1.4. Na+ channels are effectively blocked
by tetratoxin (TTX). TTX is abundly present in the overies, liver and lesser
amounts in the intestine and skin of the puffer fish (fugu; Tetradon viridis)
(Denac et al., 2000). Fish cardiac INa is always TTX sensetive, in
contrast to the mammalian cardiac INa which is about 1000 times less
sensetive to this marine toxin (Vornanen et al., 2011).

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