• Korean Journal of Animal Reproduction
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• v.26 no.2
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• pp.125-132
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• 2002

This study was conducted to examine the effects of electric stimulation conditions on in vitro developmental ability of procine embryos after somatic cell nuclear transfer, The porcine ear cell was cultured in vifro for confluency in serum-starvation condition (TCM-199＋0.5% FBS) for cell confluency. The zona pellucida of IVM oocytes were partially drilled using laser system. Single somatic cell was individually transferred into the enucleated oocyte. The reconstructed embryos were electrically fused with 0.3M mannitol. After electric fusion, the embryos were activated and cultured in NCSU-23 medium containing 10% FBS at 39$^{\circ}C$, 5% $CO_2$ in air for 6 to 8 days. Nuclear transferred(NT) oocytes which fused at a field strength of 1.90kv/cm showed a higher (P<0.05) fusion rate(49.5%, 50/101) compared to 2.10 kv/cm(25.8%, 24/93) or 2.50kv/cm(30.3%, 27/89). After electric activation, the cleavage rate of NT embryos was 48.0(24/50), 66.6(16/24) and 70.3% (19/27), respectively and these were not different. There was no significant difference in fusion rate by duration and pulse of electric stimulation. In cleavage rate, however, more NT embryos(76.3%, 45/59) cleaved at 60 $\mu$sec twice than other embryos(49.1 to 56.5%) with different conditions of electric stimulation(P<0.05). NT embryos activated at a field strength of 1.50kv/cm showed a higher developmental rate(9.8%, 5/51) than those embryos activated at 1.25kv/cm(0%) or parthenotes(6.4%, 7/109). These results suggest that some factors such as field strength, duration and pulse of electric stimulation could be affected to in vitro developmental ability of nuclear transplanted porcine embryos.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.71-80
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• 2018

In patients with epilepsy, depression is a common comorbidity but difficult to be treated because many antidepressants cause pro-convulsive effects. Thus, it is important to identify the risk of seizures associated with antidepressants. To determine whether paroxetine, a very potent selective serotonin reuptake inhibitor (SSRI), interacts with ion channels that modulate neuronal excitability, we examined the effects of paroxetine on Kv3.1 potassium channels, which contribute to high-frequency firing of interneurons, using the whole-cell patch-clamp technique. Kv3.1 channels were cloned from rat neurons and expressed in Chinese hamster ovary cells. Paroxetine reversibly reduced the amplitude of Kv3.1 current, with an $IC_{50}$ value of $9.43{\mu}M$ and a Hill coefficient of 1.43, and also accelerated the decay of Kv3.1 current. The paroxetine-induced inhibition of Kv3.1 channels was voltage-dependent even when the channels were fully open. The binding ($k_{+1}$) and unbinding ($k_{-1}$) rate constants for the paroxetine effect were $4.5{\mu}M^{-1}s^{-1}$ and $35.8s^{-1}$, respectively, yielding a calculated $K_D$ value of $7.9{\mu}M$. The analyses of Kv3.1 tail current indicated that paroxetine did not affect ion selectivity and slowed its deactivation time course, resulting in a tail crossover phenomenon. Paroxetine inhibited Kv3.1 channels in a use-dependent manner. Taken together, these results suggest that paroxetine blocks the open state of Kv3.1 channels. Given the role of Kv3.1 in fast spiking of interneurons, our data imply that the blockade of Kv3.1 by paroxetine might elevate epileptic activity of neural networks by interfering with repetitive firing of inhibitory neurons.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.112-112
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• 2003

Voltage-gated $K^{+}$ (Kv) channels represent a structurally and functionally diverse group of membrane proteins. These channels play an important role in determining the length of the cardiac action potential and are the targets for antiarrhythmic drugs. Many $K^{+}$ channel genes have been cloned from human myocardium and functionally contribute to its electrical activity. One of these channels, Kv1.5, is one of the more cardiovascular-specific $K^{+}$ channel isoforms identified to date and forms the molecular basis for an ultra-rapid delayed rectifier $K^{＋}$ current found in human atrium. Thus, the blocker of hKv1.5 is expected to be an ideal antiarrhythmic drug for atrial fibrillation. Chelidonine was isolated from Chelidonium majus L. We examined the effect of chelidonine on the hKv1.5 current expressed in Ltk-cells using whole cell mode of patch clamp techniques. Chelidonine selectively inhibited the hKv1.5 current expressed in Ltk-cells in a concentration-dependent manner, whereas did not affect the HERG current expressed in HEK-293 cells. Additionally, chelidonine reduced the tail current amplitude recorded at -50 mV after 250 ms depolarizing pulses to +60 mV, and slowed the deactivation time course resulting in a 'crossover' phenomenon when the tail currents recorded under control conditions and in the presence of chelidonine were superimposed. We found that chelidonine also inhibited the $K^{+}$ current in isolated human atrial myocytes where hKv1.5 channels were predominantly expressed. Furthermore, we examined the effects of chelidonine on the action potentials in rabbit hearts using conventional microelectrode technique. Chelidonine prolonged the action potential durations (APD) of atrial, ventricular myocytes and Purkinje fibers in a dose-dependent manner. However, the effect of chelidonine on atrial APD was frequency-dependent whereas the effect of chelidonine on the APDs of ventricular myocytes and Purkinje fibers was not frequency- dependent. Also, the selective action of chelidonine on heart was more potent than dofetilide, $K^{+}$ channel blocker.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.5
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• pp.471-479
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• 1999

The Kv channel activity in vascular smooth muscle cell plays an important role in the regulation of membrane potential and blood vessel tone. It was postulated that increased blood vessel tone in hypertension was associated with alteration of Kv channel and membrane potential. Therefore, using whole cell mode of patch-clamp technique, the membrane potential and the 4-AP-sensitive Kv current in cerebral arterial smooth muscle cells were compared between normotensive rat and one-kidney, one-clip Goldblatt hypertensive rat (lK,lC-GBH rat). Cell capacitance of hypertensive rat was similar to that of normotensive rat. Cell capacitance of normotensive rat and 1K,lC-GBH rat were $20.8{\pm}2.3$ and $19.5{\pm}1.4$ pF, respectively. The resting membrane potentials measured in current clamp mode from normotensive rat and 1K,lC-GBH rat were $-45.9{\pm}1.7$ and $-38.5{\pm}1.6$ mV, respectively. 4-AP (5 mM) caused the resting membrane potential hypopolarize but charybdotoxin $(0.1\;{\mu}M)$ did not cause any change of membrane potential. Component of 4-AP-sensitive Kv current was smaller in 1K,lC-GBH rat than in normotensive rat. The voltage dependence of steady-state activation and inactivation of Kv channel determined by using double-pulse protocol showed no significant difference. These results suggest that 4-AP-sensitive Kv channels playa major role in the regulation of membrane potential in cerebral arterial smooth muscle cells and alterations of 4-AP-sensitive Kv channels would contribute to hypopolarization of membrane potential in 1K,lC-GBH rat.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.2
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• pp.71-77
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• 2006

The goal of this study was to analyze the effects of genistein, a widely used tyrosine kinase inhibitor, on cloned Shaw-type $K^+$ currents, Kv3.1 which were stably expressed in Chinese hamster ovary (CHO) cells, using the whole-cell configuration of patch-clamp techniques. In whole-cell recordings, genistein at external concentrations from 10 to $100{\mu}M$ accelerated the rate of inactivation of Kv3.1 currents, thereby concentration-dependently reducing the current at the end of depolarizing pulse with an $IC_{50}$ value of $15.71{\pm}0.67{\mu}M$ and a Hill coefficient of $3.28{\pm}0.35$ (n=5). The time constant of activation at a 300 ms depolarizing test pulses from -80 mV to +40 mV was $1.01{\pm}0.04$ ms and $0.90{\pm}0.05$ ms (n=9) under control conditions and in the presence of $20{\mu}M$ genistein, respectively, indicating that the activation kinetics was not significantly modified by genistein. Genistein $(20{\mu}M)$ slowed the deactivation of the tail current elicited upon repolarization to -40 mV, thus inducing a crossover phenomenon. These results suggest that drug unbinding is required before Kv3.1 channels can close. Genistein-induced block was voltage-dependent, increasing in the voltage range $(-20\'mV{\sim}0\'mV)$ for channel opening, suggesting an open channel interaction. Genistein $(20{\mu}M)$ produced use-dependent block of Kv3.1 at a stimulation frequency of 1 Hz. The voltage dependence of steady-state inactivation of Kv3.1 was not changed by $20{\mu}M$ genistein. Our results indicate that genistein blocks directly Kv3.1 currents in concentration-, voltage-, time-dependent manners and the action of genistein on Kv3.1 is independent of tyrosine kinase inhibition.

• Journal of the Korean Society of Radiology
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• v.1 no.3
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• pp.5-10
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• 2007

This study was performed to measure about exposure dose during simple abdmon radiation radiography. The exposure dose was measured by PDD, surface dose, respectively. The result was as followed: 1. When tube voltage were increased with 60-85kv, surface dose were increased. When FFD(focus film distance) at the 50-150cm and mAs were increased, surface dose were decreased. 2. The percentage depth dose(PDD) were appeared 50% below depth dose at 4cm with 60-75kv, and 6cm depth with 80-85kv, 5% below depth dose at 12cm with 60kv, and depth with 65-85kv. 3. The percentage forward scatter increased from 10% to 11.78% at the 60-85kv. The back scatter dose were increase from 25% to 37% at the 60-85kv. The side scatter dose were affected to heel effect.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.6
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• pp.545-553
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• 2020

Aripiprazole is a quinolinone derivative approved as an atypical antipsychotic drug for the treatment of schizophrenia and bipolar disorder. It acts as with partial agonist activities at the dopamine D2 receptors. Although it is known to be relatively safe for patients with cardiac ailments, less is known about the effect of aripiprazole on voltage-gated ion channels such as transient A-type K⁺ channels, which are important for the repolarization of cardiac and neuronal action potentials. Here, we investigated the effects of aripiprazole on Kv1.4 currents expressed in HEK293 cells using a whole-cell patch-clamp technique. Aripiprazole blocked Kv1.4 channels in a concentration-dependent manner with an IC₅₀ value of 4.4 μM and a Hill coefficient of 2.5. Aripiprazole also accelerated the activation (time-to-peak) and inactivation kinetics. Aripiprazole induced a voltage-dependent (δ = 0.17) inhibition, which was use-dependent with successive pulses on Kv1.4 currents without altering the time course of recovery from inactivation. Dehydroaripiprazole, an active metabolite of aripiprazole, inhibited Kv1.4 with an IC₅₀ value of 6.3 μM (p < 0.05 compared with aripiprazole) with a Hill coefficient of 2.0. Furthermore, aripiprazole inhibited Kv4.3 currents to a similar extent in a concentration-dependent manner with an IC₅₀ value of 4.9 μM and a Hill coefficient of 2.3. Thus, our results indicate that aripiprazole blocked Kv1.4 by preferentially binding to the open state of the channels.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.4
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• pp.415-421
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• 2017

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent $K^+$ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The $IC_{50}$ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were $9.54{\pm}1.33{\mu}M$ and $0.75{\pm}0.10$, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.

• Bulletin of the Korean Chemical Society
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• v.17 no.12
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• pp.1123-1127
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• 1996

Crystalline compound RbV2SeO7, a Rb analogue of KV2SeO7, was synthesized from a hydrothermal reaction of V2O5, V2O3, SeO2, and Rb2CO3 in the mole ratio 3: 1: 15: 6 (in millimoles) at 230℃. RbV2SeO7 crystallizes in an orthorhombic space group Pnma (No. 62) with a=18.444(8), b=5.415(3), c=7.070(4) Å, Z=8. The two structures of KV2SeO7 and RbV2SeO7 are almost the same except that bond lengths in the latter are slightly longer than in the former. The magnetic susceptibility measurement for RbV2SeO7 in the temperature range 4-300 K showed an antiferromagnetic ordering with TN=45 K, higher than that for KV2SeO7 of 27 K. The origin of the magnetic coupling and the different ordering temperatures in the two phases are discussed in relation to the crystal structures.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.225-232
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• 2017

We demonstrated the effect of nortriptyline, a tricyclic antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent $K^+$ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent $IC_{50}$ value of $2.86{\pm}0.52{\mu}M$ and a Hill coefficient of $0.77{\pm}0.1$. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not use-dependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake.