• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.741-748
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• 1997

In the present study, we have investigated the effect of metabolic inhibition on the inward rectifier K current ($I_{K1}$). Using whole cell patch clamp technique we applied voltage ramp from +80 mV to -140 mV at a holding potential of -30 mV and recorded the whole cell current in single ventricular myocytes isolated from the rabbit heart. The current-voltage relationship showed N-shape (a large inward current and little outward current with a negative slope) which is a characteristic of $I_{K1}$. Application of 0.2 mM dinitrophenol (DNP, an uncoupler of oxidative phosphorylation as a tool for chemical hypoxia) to the bathing solution with the pipette solution containing 5 mM ATP, produced a gradual increase of outward current followed by a gradual decrease of inward current with little change in the reversal potential (-80 mV). The increase of outward current was reversed by glibenclamide ($10\;{\mu}M$), suggesting that it is caused by the activation of $K_{ATP}$. When DNP and glibenclamide were applied at the same time or glibenclamide was pretreated, DNP produced same degree of reduction in the magnitude of the inward current. These results show that metabolic inhibition induces not only the increase of $K_{ATP}$ channel but also the decrease of $I_{K1}$. Perfusing the cell with ATP-free pipette solution induced the changes very similar to those observed using DNP. Long exposure of DNP (30 min) or ATP-free pipette solution produced a marked decrease of both inward and outward current with a significant change in the reversal potential. Above results suggest that the decrease of $I_{K1}$ may contribute to the depolarisation of membrane potential during metabolic inhibition.

• Journal of Korean Neurosurgical Society
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• v.39 no.3
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• pp.215-220
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• 2006

Objective : Tyrosine kinase inhibitors may be useful in the management of cerebral vasospasm. It has not yet been reported whether L-type $Ca^{2+}$ channels playa role in tyrosine kinase inhibitors-induced vascular relaxation of cerebral artery. This study was undertaken to clarify the role of L-type $Ca^{2+}$ channels in tyrosine kinase inhibitors-induced vascular relaxation, and to investigate the effect of tyrosine kinase inhibitors on L-type $Ca^{2+}$ channels currents in freshly isolated smooth muscle cells from rat basilar artery. Methods : The isolation of rat basilar smooth muscle cells was performed by special techniques. The whole cell currents were recorded by whole cell patch clamp technique in freshly isolated smooth muscle cells from rat basilar artery. Results : Patch clamp studies revealed a whole-cell current which resembles the L-type $Ca^{2+}$ current reported by others. The amplitude of this current was decreased by nimodipine and increased by Bay K 8644. Genistein[n=5], tyrphostin A-23[n=3]. A-25[n=6] $30{\mu}M$ reduced the amplitude of the L -type $Ca^{2+}$ channel current in whole cell mode. In contrast, diadzein $30{\mu}M$ [n=3]. inactive analogue of genistein, did not decrease the amplitude of the L-type $Ca^{2+}$ channels current. Conclusion : These results suggest that tyrosine kinase inhibitors such as genistein, tyrphostin A-23, A-25 may relax cerebral vessel through decreasing level of intracellular calcium, [$Ca^{2+}$]i, by inhibition of L-type $Ca^{2+}$ channel.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.477-484
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• 1997

Intracellular recordings of oscillatory firing (bursting activity) were obtained from Purkinje cells (PCs) in rat cerebellar slices. Apamin inhibited post-burst hyperpolarizations (PBHs) progressively and finally terminated oscillatory firing activity of PCs. Apamin did not affect the amplitude or duration of the after-hyperpolarization (AHP) between spikes within the burst. In the voltage clamp mode, apamin shifted the whole-cell, quasi-steady state I/V relationship in an inward direction and abolished the zero slope resistance (ZSR) region by blocking outward current. Nickel ($Ni^{2+}$) terminated oscillatory activity and also abolished the ZSR region. However, $Ni^{2+}$ did not have progressive blocking action on the post-burst hyperpolarization before it blocked oscillatory activity. $Ni^{2+}$ blocked an inward current at potentials positive to approximately -65 mV, which was responsible for the ZSR region and outward current at more negative potentials. These data indicated that oscillatory activity of PCs is sustained by a balance between a slow $Ni^{2+}$-sensitive inward current and an apamin-sensitive outward current in the region of ZSR of the whole-cell I/V curve.

• 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.

• YAKHAK HOEJI
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• v.50 no.2
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• pp.111-117
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• 2006

Cardiac chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances. To examine a possible role of fluid pressure (FP) in the regulatien of atrial $Ca^{2+}$ signaling we investigated the effect of FP on L-type $Ca^{2+}$ current $(I_{Ca})$ in rat ventricular myocytes using whole-cell patch-clamp technique. FP $(\sim40cm\;H_2O)$ was applied to whole area of single myocytes with electronically controlled micro-jet system. FP suppressed the magnitude of peak $I_{Ca}$ by $\cong25\%$ at 0 mV without changing voltage dependence of the current-voltage relationship. FP significantly accelerated slow component in inactivation of $I_{Ca}$, but not its fast component. Analysis of steady-state inactivation curve revealed a reduction of the number of $Ca^{2+}$ channels available for activity in the presence of FP. Dialysis of myocytes with high concentration of immobile $Ca^{2+}$ buffer partially attenuated the FP-induced suppression of $I_{Ca}$. In addition, the intracellular $Ca^{2+}$ buttering abolished the FP-induced acceleration of slow component in $I_{Ca}$ inactivation. These results indicate that FP sup-presses $Ca^{2+}$ currents, in part, by increasing cytosolic $Ca^{2+}$ concentration.

• 한국태양에너지학회:학술대회논문집
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• 2008.11a
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• pp.36-41
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• 2008

In this paper, we study The Effects of PV Cell's Electrical Characteristics for PV Module Application. Photovoltaic module consists of serially connected solar cell which has low open circuit voltage and high short circuit current characteristics. The whole current flow of PV module is restricted by lowest current of one solar cell. For the experiment, we make PV module composing the solar cells that have short circuit current difference of 0%, 1%, 3% and Random. The PV module exposed about 35days, its the maximum power drop ratio was 4.282% minimum and 6.657% maximum. And PV module of low current characteristics has electrical stress from other modules. The solar cell temperature of PV module was higher compared to PV cell. To prevent early degradation, it is need to have attention to PV cell selection.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.6
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• pp.347-352
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• 2005

The effects of nitric oxide (NO) on inhibitory neurotransmitter receptors and some types of inhibitory receptors in dissociated rod bipolar cell (RBC) were investigated. In the whole cell voltage-clamping mode, the gamma-aminobutyric acid (GABA) activated current showed both sustained and transient components. GABA activated transient current was fully blocked by bicuculine, a $GABA_A$ receptor antagonist. The cis-4-aminocrotonic acid (CACA), a $GABA_C$ receptor agonist, evoked the sustained current that was not blocked by bicuculline (BIC). Glycine activated the transient current. These results indicate that the RBCs possess $GABA_A$, $GABA_C$, and glycine inhibitory receptors. Sodium nitroprusside (SNP), a NO analogue, reduced the currents activated by $GABA_A$ receptor only, however, did not reduce the currents activated by either $GABA_C$ or glycine receptors. This study signifies further that only NO depresses the fast inhibitory response activated by $GABA_A$ receptor in RBC. We, therefore, postulate that NO might depress the light-on/off transient inhibitory responses in RBCs in the rat retina.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.555-563
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• 1997

The effects of pH on $K^+$ currents were investigated in single smooth muscle cells isolated from the thoracic aorta of Wistar-Kyoto rats. Whole-cell $K^+$ currents were recorded in the conventional configuration of the voltage-clamp technique. Pinacidil (10uM) activated the whole-cell current and the pinacidil-activated current was completely inhibited by glibenclamide (10uM) , an inhibitor of ATP-sensitive $K^+$ channel ($K_{ATP}$ channel). Pinacidil-activated current was reversed at near the $K^+$ equilibrium potential. This current was time- and voltage-independent and reduced by elevating intracellular ATP. Pinacidil-activated current was reduced by lowering the external pH. However, alteration of internal pH has controversial effects on pinacidil-activated current. When the single cell was dialyzed with 0.1 mM ATP, alteration of internal pH had no effect on pinacidil-activated $K^+$ current. In the contrast, when the single cell was dialyzed with 3 mM ATP, pinacidil-activated current was increased by lowering internal pH. Our results suggest that $K^+$ channel activated by pinacidil may be $K_{ATP}$ channel and internal $H^+$ may reduce the inhibitory effect of ATP on $K_{ATP}$ channel.

• The Korean Journal of Physiology
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• v.23 no.2
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• pp.313-328
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• 1989

The electrophysiological properties of the inward current contributing to the late plateau phase of the action potential were investigated using the whole cell clamp technique and intracellular dialysis in single atrial cells isolated from the rabbit heart. The inward current was activated by various repolarizing pulses after a brief depolarizing pulse to +40 mV for 2 ms and its time course was similar to that of the late plateau of the action potential. The current was fully activated above the potential of -40 mV and abolished by intracellular EGTA. Ryanodine of $1{\mu}M$ also abolished the late plateau and the inward current. Reduced $Na_o\;to\;30%\;and\;20\;mM\;Na_1$ diminished the late plateau together with the inward current. Diltiazem blocked the activation of the current and Ni in the concentration of $40{\sim}200\;{\mu}M$ decreased the development of the late plateau and the inward current. Fully activated current-voltage relation of the inward current showed exponential voltage dependency which was steeper in more hyperplarizing range. The above findings suggest that the inward current was activated by intracellular calcium and contribute the late plateau phase of the action potential. It could be concluded that the inward current would be the inward component of Na-Ca exchange.