• Journal of Life Science
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• v.9 no.2
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• pp.15-18
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• 1999

Tempting to further understand the molecular mechanism of pharmacological action of ethanol, we investigated the acute effects of ethanol on the GABA-activated current (IGABA) of the cultured Sprague-Dawley rat hippocampal neurons in primary culture using the whole-cell patch-clamp technique. Patch-clamp recordings revealed that ethanol potentiated the Cl- current in a concentration-dependent manner(1-300mM) in the majority of the cell studied. This study demonstrates that ethanol can potentiate IGABA in mammalian central neurons.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.112-117
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• 2013

We studied the modulation of pacemaker activities by Samchulkunbi-tang (SCKB) in cultured interstitial cells of Cajal (ICC) from murine small intestine with the whole-cell patch-clamp technique. Externally applied SCKB produced membrane depolarization in the current-clamp mode. The pretreatment with $Ca^{2+}$-free solution and thapsigargin, a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker potentials and suppressed the SCKB-induced action. The application of flufenamic acid (a nonselective cation channel blocker) abolished the generation of pacemaker potentials by SCKB. However, the application of niflumic acid (a chloride channel blocker) did not inhibit the generation of pacemaker potentials by SCKB. In addition, the membrane depolarizations were inhibited by not only GDP-${\beta}$-S, which permanently binds G-binding proteins, but also U-73122, an active phospholipase C inhibitor. These results suggest that SCKB modulates the pacemaker activities by nonselective cation channels and external $Ca^{2+}$ influx and internal $Ca^{2+}$ release via G-protein and phospholipase C-dependent mechanism. Therefore, the ICC are targets for SCKB and their interaction can affect intestinal motility.

• Journal of Life Science
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• v.9 no.2
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• pp.82-85
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• 1999

The effects of ethanol on 5-hydrosytryptamine(5-HT3) receptor-mediated ion current were evaluated in whole-cell patch-clamp recordings from NCB-20 neuroblastoma cells. The physiologic and pharmacologic properties of 5-HT-activated ion current in NCB-20 cells indicated that it was mediated by 5-HT3 receptors. Ethanol(25-100mM) potentiated 5-HT3 receptor-mediated current in a concentration-dependent manner.

• Korean Journal of Acupuncture
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• v.20 no.4
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• pp.17-29
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• 2003

목적:천수근은 염증성 관절염과 염증성 장 질환 등에 사용되어왔다. 천수근이 중심회백질 신경세포에서 하행성 진통작용에 미치는 영향을 연구하였다. 방법: 중심회백질 신경세포를 분리하여 전위고정하에서 nystatin-perforated patch-clamp technique을 시행하였다. 결과: 천수근에 의하여 유발되는 이온전류는 GABA, glycine, 그리고 glutamate 수용체를 모두 활성화시켰다.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.143-150
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• 1994

The whole-cell mode of the patch clamp technique was used to study $Ca^{2+}-activated\;Cl^-\;current$ $(I_{Cl_{Ca}})$ in gastric antral myocytes. Extracellular application of caffeine evoked $Ca^{2+}-activated\;current$. In order to isolate the chloride current from background current, all known systems were blocked with specific blockers. The current-voltage relationship of caffeine-induced current showed outward rectification and it reversed at around $E_{Cl^-}$. The shift of reversal potential upon the alteration of external and internal chloride concentrations was well fitted with results which were calculated by the Nernst equation. Extracellular addition of N-phenylanthranilic acid and niflumic acid which are known anion channel blockers abolished the caffeine induced current. Intracellular application of a high concentration of EGTA also abolished this current. Application of c-AMP, c-GMP, heparin, or $AIF^-_4$ made no remarkable changes to this current. Sodium replacement with the impermeable cation N-methylglucamine or with $Cd^{2+}$ rarely affected this current. From the above results it is suggested that the caffeine induced current was a $Cl^-$ current and it was activated by intracellular $Ca^{2+}$.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.2
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• pp.147-156
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• 2001

It has been proposed that $Ca^{2+}-activated$ K $(K_{Ca})$ channels play an essential role in vascular tone. The alterations of the properties of coronary $K_{Ca}$ channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present studies were carried out to determine the properties of coronary $K_{Ca}$ channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the present study are as follows: (1) the unitary current amplitudes and the slope conductance of coronary $K_{Ca}$ channels were decreased without changes of the channel kinetics in isoproterenol-induced cardiac hypertrophy; (2) the sensitivity of coronary $K_{Ca}$ channels to the changes of intracellular concentration of $Ca^{2+}$ was reduced in isoproterenol-induced cardiac hypertrophy. From above results, we suggest for the first time that the alteration of $K_{Ca}$ channels are involved in impaired coronary reserve in isoproterenol-induced cardiac hypertrophy.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.4
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• pp.301-309
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• 2000

The purpose of our investigation was to examine the effects of prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ on membrane potentials, $Ca^{2+}-activated\;K^+\;(K_{Ca})$ channels, and delayed rectifier $K^+(K_V)$ channels using the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells. $PGF_{2{\alpha}}$ significantly hyperpolarized membrane potentials and increased outward whole-cell K currents. $PGF_{2{\alpha}}$ increased open-state probability of $K_{Ca}$ channels without the change of the open and closed kinetics. $PGF_{2{\alpha}}$ increased the amplitudes of $K_V$ currents with a leftward shift of activation and inactivation curves and a decrease of activation time constant. Our results suggest that the activation of $K_{Ca}$ and $K_V$ channels, at least in part, may lead to attenuate or counteract vasoconstriction by $PGF_{2{\alpha}}$ in middle cerebral artery.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.581-589
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• 1998

A regulating mechanism of the ATP-sensitive potassium channels $(K_{ATP}\;channels)$ is yet to fully explained. This study was carried out to investigate the effects of intracellular application of monocarboxylates (acetate, formate, lactate, and pyruvate) on $K_{ATP}$ channels in isolated rabbit ventricular myocytes. Single channel currents of $K_{ATP}$ channels were recorded using the excised inside-out or permeabilized attached (open-cell) patch-clamp technique at room temperature. Intracellular application of acetate, formate and pyruvate led to an inhibition of channel activity, whereas intracellular application of lactate increased channel activity. These effects were reversible upon washout. Analysis of single channel kinetics showed that monocarboxylates did not affect open-time constant and close-time constant. These results suggest that monocarboxylates participate in modulating $K_{ATP}$ channels activity in cardiac cells and that modulation of $K_{ATP}$ channels activity may resolve the discrepancy between the low $K_i$ in excised membrane patches and high levels of intracellular ATP concentration during myocardial ischemia or hypoxia.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.1
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• pp.15-20
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• 2007

To investigate whether hydrogen peroxide($H_2O_2$) affects intestinal motility, pacemaker currents and membrane potential were recorded in cultured interstitial cells of Cajal(ICC) from murine small intestine by using a whole-cell patch clamp. In whole cell patch technique at $30^{\circ}C$, ICC generated spontaneous pacemaker potential under current clamp mode(I=0) and inward currents(pacemaker currents) under voltage clamp mode at a holding potential of -70 mV. When ICC were treated with $H_2O_2$ in ICC, $H_2O_2$ hyperpolarized the membrane potential under currents clamp mode and decreased both the frequency and amplitude of pacemaker currents and increased the resting currents in outward direction under voltage clamp mode. Also, $H_2O_2$ inhibited the pacemaker currents in a dose-dependent manner. Because the properties of $H_2O_2$ action on pacemaker currents were same as the effects of pinacidil(ATP-sensitive $K^+$ channels opener), we tested the effects of glibenclamide(ATP-sensitive $K^+$ channels blocker) on $H_2O_2$ action in ICC, and found that the effects of $H_2O_2$ on pacemaker currents were blocked by co- or pre- treatment of glibenclamide. These results suggest that $H_2O_2$ inhibits pacemaker currents of ICC by activating ATP-sensitive $K^+$ channels.

• Progress in Medical Physics
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• v.3 no.2
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• pp.43-57
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• 1992

Phase detector techique provides a unique probe to membrane recycling phenomenon by enabling dynamic monitoring of cell membrane capacitance. However, it has inherent errors due to constant changes in measurement environments. The present study analyzed several error sources to develope application criteria of this technique. and the following was found based on a theoretical analysis. The initial phase angle has to be appropriately selected to minimize the error due to perturbation of access and membrane conductances. Excitation frequency is also important to determine the initial phase angle. However. deviation of the phase angle from a predetermined initial value during the measurement period does not affect capacitance estimation to a significant degree. Despite an appropriate initial phase selection an error in scaling factor is expected for a large increase in capacitance during exocytosis. which may be overcome by iteratively correcting the scaling factor over the measurement period. These results will provide a useful guideline in practical application of this technique.