Sodium-activated Potassium Current in Guinea pig Gastric Myocytes

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China
Journal of Korean Medical Science (Impact Factor: 1.27). 03/2007; 22(1):57-62. DOI: 10.3346/jkms.2007.22.1.57
Source: PubMed


This study was designed to identify and characterize Na+-activated K+ current (I(K(Na))) in guinea pig gastric myocytes under whole-cell patch clamp. After whole-cell configuration was established under 110 mM intracellular Na+ concentration ([Na+]i) at holding potential of -60 mV, a large inward current was produced by external 60 mM K+([K+]degrees). This inward current was not affected by removal of external Ca2+. K+ channel blockers had little effects on the current (p>0.05). Only TEA (5 mM) inhibited steady-state current to 68+/-2.7% of the control (p<0.05). In the presence of K+ channel blocker cocktail (mixture of Ba2+, glibenclamide, 4-AP, apamin, quinidine and TEA), a large inward current was activated. However, the amplitude of the steady-state current produced under [K+]degrees (140 mM) was significantly smaller when Na+ in pipette solution was replaced with K+- and Li+ in the presence of K+ channel blocker cocktail than under 110 mM [Na+]i. In the presence of K+ channel blocker cocktail under low Cl- pipette solution, this current was still activated and seemed K+-selective, since reversal potentials (E(rev)) of various concentrations of [K+]degrees-induced current in current/voltage (I/V) relationship were nearly identical to expected values. R-56865 (10-20 microM), a blocker of I(K(Na)), completely and reversibly inhibited this current. The characteristics of the current coincide with those of I(K(Na)) of other cells. Our results indicate the presence of I(K(Na)) in guinea pig gastric myocytes.

Download full-text


Available from: PubMed Central · License: CC BY-NC
  • Source
    • "Although the major focus of studies of KNa currents has been in the nervous system, KNa channels have been described in a variety of cardiac cells including guinea pig myocytes and rat myoblasts [7, 33, 34]. They have also been found in guinea pig gastric myocytes [35] mouse diaphragm muscle [36], circular smooth muscle of the opossum lower esophageal sphincter [37], and the thick ascending limb of mouse kidney [38], as well as in Xenopus oocytes [39]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The Slack and Slick genes encode potassium channels that are very widely expressed in the central nervous system. These channels are activated by elevations in intracellular sodium, such as those that occur during trains of one or more action potentials, or following activation of non-selective cationic neurotransmitter receptors such as AMPA receptors. This review covers the cellular and molecular properties of Slack and Slick channels and compares them with findings on the properties of sodium-activated potassium currents (termed KNa currents) in native neurons. Human mutations in Slack channels produce extremely severe defects in learning and development, suggesting that KNa channels play a central role in neuronal plasticity and intellectual function.
    Full-text · Article · Apr 2013
  • Source
    • "A class of potassium channels reversibly activated by intracellular Na ϩ ions (K Na channels) were first described in inside-out patch recording of cardiac myocytes of guinea pig and were found to have high unitary K ϩ conductance (Kameyama et al., 1984). Similar single K Na channel activity was observed later in several types of neurons (Bader et al., 1985; Dryer et al., 1989; Egan et al., 1992a,b; Haimann et al., 1992; Koh et al., 1994; Safronov and Vogel, 1996; Bischoff et al., 1998; Hess et al., 2007) and other excitable and nonexcitable tissues (Rodrigo and Chapman, 1990; Wang et al., 1991; Niu and Meech, 2000; Paulais et al., 2006; Kim et al., 2007; Zhang and Paterson, 2007). A variety of studies have now shown that K Na channels contribute to slow afterhyperpolarizations that follow bursts of action potentials in neurons (Safronov and Vogel , 1996; Yang et al., 2007). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Potassium channels activated by intracellular Na(+) ions (K(Na)) play several distinct roles in regulating the firing patterns of neurons, and, at the single channel level, their properties are quite diverse. Two known genes, Slick and Slack, encode K(Na) channels. We have now found that Slick and Slack subunits coassemble to form heteromeric channels that differ from the homomers in their unitary conductance, kinetic behavior, subcellular localization, and response to activation of protein kinase C. Heteromer formation requires the N-terminal domain of Slack-B, one of the alternative splice variants of the Slack channel. This cytoplasmic N-terminal domain of Slack-B also facilitates the localization of heteromeric K(Na) channels to the plasma membrane. Immunocytochemical studies indicate that Slick and Slack-B subunits are coexpressed in many central neurons. Our findings provide a molecular explanation for some of the diversity in reported properties of neuronal K(Na) channels.
    Full-text · Article · May 2009 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
  • [Show abstract] [Hide abstract]
    ABSTRACT: The slack (slo2.2) gene codes for a potassium-channel α-subunit of the 6TM voltage-gated channel family. Expression of slack results in Na(+)-activated potassium channel activity in various cell types. We describe the purification and reconstitution of Slack protein and show that the Slack α-subunit alone is sufficient for potassium channel activity activated by sodium ions as assayed in planar bilayer membranes and in membrane vesicles.
    No preview · Article · Jun 2012 · Journal of Membrane Biology
Show more