A persistent sodium current in rat ventricular myocytes.

Abstract

SUMMARY1. The tight seal, whole-cell, voltage-clamp technique was used to record currents from single ventricular myocytes acutely dissociated from adult rat hearts. Subtraction of currents recorded in the presence and absence of tetrodotoxin (TTX, 50 /SM) revealed a small, persistent, inward current following a much larger, transient, inward current.2. Both currents were sodium currents because they reversed close to the sodium equilibrium potential and were depressed when choline was substituted for extracellular sodium.3. The persistent sodium current could be recorded when the transient current had been inactivated with conditioning depolarization. Only slight inactivation of the persistent current occurred during depolarizing pulses lasting up to 900 ms. 4. A lower concentration of TTX (0-1 /,lM) blocked the persistent sodium current while having little effect on the transient sodium current.5. The persistent sodium current was activated at more negative potentials than the transient sodium current. It cannot have been a window current because it was recorded at positive potentials when the transient current was completely inactivated.6. Because the persistent and transient sodium currents had a different voltage dependence and sensitivity to TTX, it was concluded that different channels are responsible for the two currents.

Identification of rhythmically active cells in guinea‐pig stomach

“…Another set of voltagedependent channels might be involved. However, although channels which will support long lasting depolarizations have been demonstrated in cardiac muscle (Saint et al 1992), they have not been demonstrated in antral smooth muscle cells (Noack et al 1992). The alternative possibility is that the regenerative component arises from the regenerative release of Ca¥ from an internal store (Fabiato & Fabiato, 1975) and this activates a set of channels which causes an increase in the net positive internal charge (see as examples Pacaud & Bolton, 1991;Large & Wang, 1996;Hashitani, et al 1996).…”

Potent block of inactivation-deficient Na+ channels by n-3 polyunsaturated fatty acids

“…3, 5, and 7). The persistent I Na current has been observed in adult mammalian ventricular cardiomyocytes (14), and hypoxia has been shown to enhance its amplitude (5). Increased Na ϩ influx during hypoxia increases intracellular Na ϩ concentration ([Na ϩ ] i ), which in turn activates the reversal mode of the Na ϩ /Ca 2ϩ exchanger so that intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) level increases as well.…”

“…How the mutant L409C/A410W produces an inactivationdeficient channel, which it does (14), must be different from that produced by the inactivation-dependent mutant IFMQ3. It has been postulated that the mutant L409C/A410W composes part of the receptor site for the docking of the inactivation particle (15).…”

Molecular Diversity of Structure and Function of the Voltage-Gated Na+ Channels

“…+ currents in neurons Persistent (noninactivating) Na + currents flowing at subthreshold potentials have been recorded in various tissues such as frog node of Ranvier (19), cat lumbar motoneurons (20), rat and guinea pig hippocampal neurons (21), rat ventricular myocytes (22), rat optic nerve axons (23), rat and cat cortical pyramidal neurons (24), guinea pig trigeminal motoneurons (25), rat dorsal root ganglion (DRG) neurons (26) and guinea pig cerebellar Purkinje cells (27).…”