. 2010 Mar 19;8(3):741–762. doi: 10.3390/md8030741

Table 1.

Suggested functions of TTXs Na⁺ channels in the mammalian myocardium. A detailed overview on tissue distribution and detection methods for the individual TTXs Na⁺ channels was given by Haufe et al. [9].

Study	Results and suggested function of TTXs Na⁺ channels	Species
	*Sinus node automaticity and control of heart rate*
[13,14]	Na_v1.1 transcripts and TTXs currents (IC₅₀ ~ 26 nM) in newborn (but not adult) sinus node cells, suggesting that, depending on age, TTXs Na⁺ channels contribute to slow diastolic depolarization.	Rabbit
[12]	Reduction in spontaneous heart rate by blocking Na_v1.1/Na_v1.3 at 100 nM TTX; important contribution of TTXs Na⁺ channels to sinus node automaticity and rhythm, suggesting a possible contribution to SSS in man.	Mouse
[15]	Slowing of pacemaking in intact sinus node preparations and isolated cells at 10 and 100 nM TTX, slowing of both pacemaking and sinus node conduction at 1–30 μM TTX.	Mouse

	*Efficient EC coupling and increased cardiac contractility*
[11]	Reduction of left ventricular function at 100 and 200 nM TTX, suggesting an unexpected role of brain-type Na⁺ channels in excitation-contraction coupling.	Mouse, guinea pig
[16]	Localization of brain-type Na⁺ channels and two β subunits in transverse tubules of myocytes, suggesting AP propagation from the cell surface into the interior by defined α/β-channel complexes.	Mouse

	*Purkinje fibers: Efficient cardiac conduction and AP prolongation*
[17]	Shortening of AP duration, but not of the maximum rate of rise, at low TTX (≥33 nM).	Dog
[18]	Higher transcript levels and TTXs currents in Purkinje fibers (35 and 22%), when compared to ventricular myocytes (<20 and 10%, respectively).	Dog
[19]	Expression of Na_v1.4 in cardiac Purkinje myocytes (PCR, immunofluorescence).	Dog

	*Other reports*
[20]	Detection of Na_v1.1 transcripts in the heart.	Rat
[21]	Cardiac Na⁺ channels are composed of either Na_v1.1 or Na_v1.5, and both associate with β1 and β2.	Mouse, rat
[22]	Up-regulation of Na_v1.1 and increased TTXs Na⁺ current in the postinfarction remodeled myocardium.	Rat
[5,23]	Large transcript pool in whole hearts (30–40%), smaller TTXs Na⁺ currents in ventricular myocytes (8%) of mice (not observed in pigs and humans).	Mouse
[10]	Middle region of ventricular myocytes contains only TTXs Na⁺ channels, that can be blocked by 50 nM TTX.	Rabbit
[24]	Prolongation of the cycle length of the spontaneous pacemaker activity at 100 nM TTX by 22% and 53% in sinoatrial and atrioventricular node preparations, respectively.	Mouse