• The Korean Journal of Physiology and Pharmacology
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• v.4 no.4
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• pp.333-338
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• 2000

We have examined whether bile acids can affect the electrical and mechanical activities of circular smooth muscle of canine colon and ileum, using isometric tension measurement or patch clamp technique. It was found that a dilution of canine bile $(0.03{\sim}2%\;by\;volume)$ enhanced or inhibited the amplitude of spontaneous contractions. An individual component of bile, deoxycholic acid (DCA) enhanced the frequency and amplitude of the spontaneous contractile activity at $10^{-6}\;M,$ while DCA at $10^{-4}\;M$ inhibited the contraction. Similarly, the response to cholic acid was excitatory at $10^{-5}\;M$ and inhibitory at $3{\times}10^{-4}\;M.$ Taurocholic acid at $10^{-4}\;M$ enhanced the amplitude of muscle contraction. Electrically, canine bile at 1% reversibly depolarized the colonic myocytes under current clamp mode. Bile acids also elicited non-selective cation currents under voltage clamp studies, where $K^+$ currents were blocked and the $Cl^-$ gradient was adjusted so that $E_{Cl}^-$ was equal to -70 mV, a holding potential. The non-selective cation current might explain the depolarization caused by bile acids in intact muscles. Furthermore, the bile acid regulation of electrical and mechanical activities of intestinal smooth muscle may explain some of the pathophysiological conditions accompanying defects in bile reabsorption.

• The Korean Journal of Physiology
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• v.27 no.2
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• pp.115-122
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• 1993

There is evidence that noradrenaline enhances spontaneous contractions dose-dependently in guinea-pig antral circular muscle. To investigate the mechanism of this excitatory action, slow waves and membrane currents were recorded using conventional microelectrode techniques in muscle strips and the whole cell patch clamp technique in isolated gastric myocytes. On recording slow waves, noradrenaline $(10^{-5}\;M)$ induced the hyperpolarization of the membrane potential, although the shape of the slow waves became tall and steep. Also, spike potentiaIs occurred at the peaks of slow waves. These changes were completely reversed by administration of phentolamine $(10^{-5}\;M),\;an\;{\alpha}-adrenoceptor$ blocker. Noradrenaline-induced hyperpolarization was blocked by apamin $(10^{-7}\;M)$, a blocker of a class of $Ca^{2+}\;-dependent\;K^+$ channels. To investigate the mechanisms for these effects, we performed whole cell patch clamp experiments. Norndrenaline increased voltage-dependent $Ca^{2+}$ currents in the whole range of test potentials. Noradrenaline also increased $Ca^{2+}\;-dependent\;K^+$\;currents, and this effects was abolished by apamin. These results suggest that the increase in amplitude and the generation of spike potentials on slow waves was caused by the activation of voltage-dependent $Ca^{2+}$ channel via adrenoceptors, and hyperpolarization of the membrane potential was mediated by activation of apamin-sensitive $Ca^{2+}\;-dependent\;K^+\;channels$.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.131-135
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• 2008

The profile of membrane currents was investigated in differentiated neuronal cells derived from human neural stem cells (hNSCs) that were obtained from aborted fetal cortex. Whole-cell voltage clamp recording revealed at least 4 different currents: a tetrodotoxin (TTX)-sensitive $Na^+$ current, a hyperpolarization-activated inward current, and A-type and delayed rectifier-type $K^+$ outward currents. Both types of $K^+$ outward currents were blocked by either 5 mM tetraethylammonium (TEA) or 5 mM 4-aminopyridine (4-AP). The hyperpolarization-activated current resembled the classical $K^+$ inward current in that it exhibited a voltage-dependent block in the presence of external $Ba^{2+}$ (30 ${\mu}$M) or $Cs^+$ (3${\mu}$M). However, the reversal potentials did not match well with the predicted $K^+$ equilibrium potentials, suggesting that it was not a classical $K^+$ inward rectifier current. The other $Na^+$ inward current resembled the classical $Na^+$ current observed in pharmacological studies. The expression of these channels may contribute to generation and repolarization of action potential and might be regarded as functional markers for hNSCs-derived neurons.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.361-368
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• 1998

The spontaneous contractions of gastric smooth muscles are regulated by slow waves, which are modulated by both nervous system and humoral agents. This study was designed to examine the effects of prostaglandin $E_2$ ($PGE_2$) on the contractile and electrical activities of antral smooth muscles in guinea-pig stomach, using an intracellular recording technique. To elucidate the underlying mechanism for its effect on contractility, ionic currents were also measured using a whole-cell patch clamp method. The basal tone by $PGE_2$ was variable, whereas the magnitude of phasic contractions was reduced ($19.0{\pm}2.1%$, n=19). The resting membrane potentials were hyperpolarized ($-4.4{\pm}0.5%$ mV, n=10), and plateau potentials were lowered ($-2.9{\pm}0.5%$ mV, n=10). In most cases, however, the initial peak potentials of slow waves were depolarized more by $PGE_2$ than those of control. The frequency of the slows wave was increased from $5.7{\pm}0.2$ cycles/min to $6.5{\pm}0.2$ (n=22). Voltage-operated $Ca^{2+}$ currents were decreased by $PGE_2$ (n=5). Voltage-operated $K^+$ currents, both Ca-dependent and Ca-independent, were increased (n=5). These results suggest that $PGE_2$ plays an important role in the modulation of gastric smooth muscle activities, and its inhibitory effects on the contractility and activities of slow waves are resulted from both decrease of $Ca^{2+}$ currents and increase of $K^+$ currents.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2013.05a
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• pp.531-533
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• 2013

In this paper, to study the IPMC (Ionic exchange Polymer Metal Composite) material consisting of a sulfonic acid ion and fluoride combination of carbon with Nafion film greatly affected the electro-active polymer (Electro Active Polymer) characteristics and the presence of water and cationshave properties. Use or electrical energy into mechanical energy, mechanical energy, electrical energy, and can be utilized to its characteristics, depending on the water and cations in water varies greatly. Configure the device simulations in order to study the electrical properties of these IPMC. Stepper Motor using MCU and simulator designed for the electrical characterization due to the movement and to the implementation of the mechanical movement of ocean currents. In this study, configuration the IPMC and simulation device to the area of the IPMC to the efficient use of energy currents, frequency, salinity concentration, through the efficient use of the IPMC due to the bend angle of the electrical analysis and research methods we propose.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.2
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• pp.189-197
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• 2001

To investigate propofol's effects on ionic currents induced by ${\gamma}-aminobutyric$ acid (GABA) and glycine as well as on those produced by the nicotinic acetylcholine- and glutamate-responsive channels, rat dorsal raphe neurons were acutely dissociated and the nystatin-perforated patch-clamp technique under voltage-clamp conditions was used to observe their responses to the administration of propofol. Propofol evoked ion currents in a dose-dependent manner, and propofol $(10^{-4}\;M)$ was used to elicit ion currents through the activation of $GABA_A,$ glycine, nicotinic acetylcholine and glutamate receptors. Propofol at a clinically relevant concentration $(10^{-5}\;M)$ potentiated $GABA_A-,$ glycine- and NMDA receptor-mediated currents. The potentiating action of propofol on $GABA_A-,$ glycine- and NMDA receptor-mediated responses involved neither opioid receptors nor G-proteins. Apparently, propofol modulates inhibitory and excitatory neurotransmitter-activated ion channels either by acting directly on the receptors or by potentiating the effects of the neurotransmitters, and this modulation appears to be responsible for the majority of the anaesthetic and/or adverse effects.

• The Korean Journal of Physiology
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• v.26 no.1
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• pp.27-35
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• 1992

We used the whole cell patch clamp technique to examine the ionic basis for the tail current after depolarizing pulse in single atrial myocytes of the rabbit. We recorded the tail currents during various repolarizations after short depolarizing pulse from a holding potential of -70 mV. The potassium currents were blocked by external 4-aminopyridine and replacement of internal potassium with cesium. The current was reversed to the outward direction above +10 mV. High concentrations of intracellular calcium buffer inhibited the activation of the current. Diltiazem and ryanodine blocked it too. These data suggest that the current is activated by intracellular calcium released from sarcoplasmic reticulumn. When the internal chloride concentration was increased, the inward tail current was increased. The current was partially blocked by the anion transport blocker niflumic acid. The current voltage curve of the niflumic acid sensitive current component shows outward rectification and is well fitted to the current voltage curve of the theoretically predicted chloride current calculated from the constant field equation. The currents recorded in rabbit atrial myocytes, with the method showing isolated outward Na Ca exchange current in ventricular cells of the guinea pig, suggested that chloride conductance could be activated with the activation of Na/ca exchange current. From the above results it is concluded that a chloride sensitive component which is activated by intracellular calcium contributes to tail currents in rabbit atrial cells.

• Journal of the Korean Electrochemical Society
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• v.6 no.2
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• pp.98-102
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• 2003

Urethane acrylate oligomer was synthesized and used in a gel polymer electrolyte (GPE) and then its electrochemical performances were evaluated. $LiCoO_2/GPE/graphite$ cells were prepared and their performances depending on discharge currents and temperatures were evaluated. The precursor containing $5 vol\%$ curable mixture had a low viscosity relatively. ionic conductivity of the gel polymer electrolyte at room temperature and $-20^{\circ}C$ was ca. $5.9\times10^{-3}S{\cdot}cm^{-1}\;and\;1.4times10^{-3}S{\cdot}cm^{-1}$, respectively. GPE showed good electrochemical stability up to potential of 4.5V vs. RLi/Li^+.\;LiCoO_2/GPE/graphite$ cell showed a good high-rate and low-temperature performance.

• Journal of the Korean Vacuum Society
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• v.18 no.3
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• pp.197-202
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• 2009

The long term stability of ion current of QMS has been one of key parameters for monitoring gas process in vacuum. The time dependence of ionic current was monitored while the pressure of nitrogen gas was kept at a fixed pressure by introducing the gas into vacuum chamber. The chamber was evacuated to ${\sim}3{\times}10^{-9}\;Torr$ to reduce background signals before the measurement. Two ion sources were tested; one had brownish or black color due to gas contamination and the other one was new, i.e. cleaner. At a nitrogen pressure of $1{\times}10^{-5}\;Torr$, the ionic currents measured by the contaminated ion source decreased faster with time. The decrease rate was respectively ${\sim}46%$ for cleaner one and ${\sim}84%$ for contaminated one after ${\sim}5.5%$ hours. In order to test the effect of filament material on the ion current decrease, we fabricated a tungsten(W) filament which consisted of two parts; one half was made of W and the other was coated with yttria. The similar decrease of ionic currents were shown for the two types of filaments, indicating that slight change of temperature of filament due to material difference i.e. baking effect could not improve the origin of ionic current decrease. Overall the decreasing rate of ionic current is more closely associated with contaminated ion source of QMS rather than its filament materials.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.623-630
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• 1999

Decreased cardiac contractility occurs in endotoxicosis, but little is known about the ionic mechanism responsible for myocardial dysfunction. In this study, we examined the changes in $Ca{2+}$ and $K^+$ currents in cardiac myocytes from endotoxin-treated rat. Ventricular myocytes were isolated from normal and endotoxemic rats (ex vivo), that were treated for 10 hours with Salmonella enteritidis lipopolysaccharides (LPS; 1.5 mg/kg) intravenously. Normal cardiac myocytes were also incubated for 6 hours with 200 ng/ml LPS (in vitro). L-type $Ca{2+}$ current $(I_{Ca,L})$ and transient outward $K^+$ current $(I_{to})$ were measured using whole cell patch clamp techniques. Peak $I_{Ca,L}$ was reduced in endotoxemic myocytes (ex vivo; 6.00.4 pA/pF, P＜0.01) compared to normal myocytes (control; 10.90.6 pA/pF). Exposure to endotoxin in vitro also attenuated $I_{Ca,L}$ (8.40.4 pA/pF, P＜0.01). The amplitude of $(I_{to})$ on depolarization to 60 mV was reduced in endotoxin treated myocytes (16.51.5 pA/pF, P＜0.01, ex vivo; 20.00.9 pA/pF, P＜0.01 , in vitro) compared to normal myocytes (control; 24.71.0 pA/pF). There was no voltage shift in steady-state inactivation of $I_{Ca,L}$ and $(I_{to})$ between groups. These results suggest that endotoxin reduces $Ca{2+}$ and $K^+$ currents of rat cardiac myocytes, which may lead to cardiac dysfunction.