• Development and Reproduction
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• v.21 no.1
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• pp.11-18
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• 2017

Potassium channels, the largest group of pore proteins, selectively regulate the flow of potassium ($K^+$) ions across cell membranes. The activity and expression of $K^+$ channels are critical for the maintenance of normal functions in vessels and neurons, and for the regulation of cell differentiation and maturation. However, their role and expression in stem cells have been poorly understood. In this study, we isolated perivascular stem cells (PVCs) from human umbilical cords and investigated the expression patterns of big-conductance $Ca^{2+}$-activated $K^+$ ($BK_{Ca}$) and voltage-dependent $K^+$ ($K_v$) channels using the reverse transcription polymerase chain reaction. We also examined the effect of high glucose (HG, 25 mM) on expression levels of $BK_{Ca}$ and $K_v$ channels in PVCs. $K_{Ca}1.1$, $K_{Ca}{\beta}_3$, $K_v1.3$, $K_v3.2$, and $K_v6.1$ were detected in undifferentiated PVCs. In addition, HG treatment increased the amounts of $BK_{Ca}{\beta}_{3a}$, $BK_{Ca}{\beta}_4$, $K_v1.3$, $K_v1.6$, and $K_v6.1$ transcripts. These results suggested that ion channels may have important functions in the growth and differentiation of PVCs, which could be influenced by HG exposure.

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.42-42
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• 2003

Large-conductance $Ca^{2+}$-activated potassium channels ($BK_{Ca}$ are a widely distributed and play key roles in various cell functions. In nerve cells, $BK_{Ca}$ channels shorten the duration of action potentials and block $Ca^{2+}$ entry thereby repolarizing excitable cells after excitation. $BK_{Ca}$ channel opening has been postulated to confer neuroprotection during stroke, and has attracted attention as a means for therapeutic intervention in asthma, hypertension, convulsions, and traumatic brain injury. Several natural and synthetic compounds including a steroid hormone, $\beta$-estradiol, have been identified as the activators of $BK_{Ca}$ channels. Based on the structural features of the previously reported activators of $BK_{Ca}$ channels, we designed several lead compounds, synthesized chemically, and tested their functional activity on cloned $BK_{Ca}$ channels. The $\alpha$ subunit of rat $BK_{Ca}$ channel was expressed alone or with different $\beta$ subunits in Xenopus oocytes and the effects of the compounds were tested electrophysiological means. One of the lead compounds affected the activity of the $\alpha$ subunit of $BK_{Ca}$ channel in a $\beta$ subunit-specific manner. While the activity of B $K_{ca}$ channel $\alpha$ subunit was Potentiated, the channel composed of $\alpha$ and $\beta$1 subunits were inhibited by this compound. We are currently investigating the mechanism of the $\beta$ subunit-dependent effects and planning to localize the receptor site of the lead compound.f the lead compound.

• International Journal of Oral Biology
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• v.40 no.4
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• pp.211-216
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• 2015

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium ($BK_{ca}$) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of $Ca^{2+}$ that induces $Ca^{2+}$-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective $BK_{Ca}$ channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove $Ca^{2+}$ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through $BK_{ca}$ channels, which are activated by intracellular $Ca^{2+}$ increase via activation of RyR of $Ca^{2+}$ stores.

• The Korean Journal of Emergency Medical Services
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• v.24 no.3
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• pp.155-160
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• 2020

Torsades de pointes refers to polymorphic ventricular tachycardia (PMVT), which is caused by the suppression of potassium channels owing to genetic and electrolytic abnormalities, resulting in the extension of the QT interval. Symptoms range from spontaneous circulation recovery to fainting and sudden death. Defibrillation, magnesium correction, and the use of lidocaine as an antiarrhythmic agent are recommended as treatments for persistent torsades de pointes. Currently, only amiodarone is available in the ambulance; however, torsades de pointes does not respond efficiently to amiodarone because it suppresses potassium channels and increases the refractory period of the myocardium. Lidocaine, in contrast, reduces the relative refractory period of the myocardium caused by suppressing sodium channels; thus, it inhibits the occurrence of and treats arrhythmia. In cases where PMVT did not respond to defibrillation, the administration of lidocaine showed no difference in survival and discharge rates compared to amiodarone. Thus, ambulances must be equipped with provisions to administer lidocaine.

• Proceedings of the IEEK Conference
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• 2004.08c
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• pp.787-791
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• 2004

We investigated field-effect ion-transport devices based on carbon nanotubes by using classical molecular dynamics simulations under applied external force fields, and we present model schematics that car be applied to the nanoscale data storage devices and unipolar ionic field-effect transistors. As the applied external force field is increased, potassium ions rapidly flow through the nanochannel. Under low external force fields, ther nal fluctuations of the nanochannels affect tunneling of the potassium ions whereas the effects of thermal fluctuations are negligible under high external force fields. Since the electric current conductivity increases when potassium ions are inserted into fullerenes or carbon nanotubes, the field effect due to the gate, which can modify the position of the potassium ions, changes the tunneling current between the drain and the source.

• BMB Reports
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• v.43 no.10
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• pp.677-682
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• 2010

Kv4.2, a pore-forming $\alpha$-subunit of voltage-gated A-type potassium channels, is expressed abundantly in the soma and dendrites of hippocampal neurons, and is responsible for somatodendritic $I_A$ current. Recent studies have suggested that changes in the surface levels of Kv4.2 potassium channels might be relevant to synaptic plasticity. Although the function and expression of Kv4.2 protein have been extensively studied, the dendritic localization of Kv4.2 mRNA is not well described. In this study, Kv4.2 mRNAs were shown to be localized in the dendrites near postsynaptic regions. The dendritic transport of Kv4.2 mRNAs were mediated by microtubule-based movement. The 500 nucleotides of specific regions within the 3'-untranslated region of Kv4.2 mRNA were found to be necessary and sufficient for its dendritic localization. Collectively, these results suggest that the dendritic localization of Kv4.2 mRNAs might regulate the dendritic surface level of Kv4.2 channels and synaptic plasticity.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.1
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• pp.25-31
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• 2000

ATP-sensitive potassium channels ($K_{ATP}$ channels) play an important role in insulin secretion from pancreatic beta cells. We have investigated the effect of propofol on $K_{ATP}$ channels in cultured single pancreatic beta cells of rats. Channel activity was recorded from membrane patches using the patch-clamp technique. In the inside-out configuration bath-applied propofol inhibited the $K_{ATP}$ channel activities in a dose-dependent manner. The half-maximal inhibition dose (ED50) was $48.6{\pm}8.4\;{\mu}M$ and the Hill coefficient was $0.73{\pm}0.11.$ Single channel conductance calculated from the slope of the relationship between single channel current and pipette potential $(+20{\sim}+100\;mV)$ was not significantly altered by propofol $(control:\;60.0{\pm}2.7\;pS,\;0.1\;mM\;propofol:\;58.7{\pm}3.5\;pS).$ However, mean closed time was surely increased. Above results indicate that propofol blocks the $K_{ATP}$ channels in the pancreatic beta cells in the range of its blood concentrations during anesthesia, suggesting a possible effect on insulin secretion and blood glucose level.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.245-254
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• 1995

The density of ATP-sensitive potassium($K_{APT}$) channels, that open as intracellular ATP concentration falls below a critical level, is very high in skeletal muscle surface membrane and those high density may imply that $K_{ATP}$ channels have very important physiological roles. To elucidate a role of $K_{ATP}$ in relation to fatigue, the modulating effects of potassium channel openers and blockers on the fatigue velocity(FV) of mouse extensor hallucis longus muscle(EHL) were investigated in vitro. Twitch contraction was induced by an electrical field stimulation (EFS: 24-48V, 20ms, 0.2-4Hz) and resulting contraction force was isometrically recorded. The twitch forces were gradually decreased to 25% of initial contraction force(ICF) in $37.52{\pm}1.55sec$($mean{\pm}s.e.m.$, n=135), indicating the fatigue phenomena. The mean velocity for development of the fatigue was measured during the period that twitch force decreased to half($FV_{0/0.5}$) and during the period from half to 25%($FV_{0.5/0.25}$) of ICF. The fatigue was induced once every one hour and the tissue response was stable for up to 4 hours. In control condition, ICF was $5.8{\pm}0.12g$ (n=144) and decreased to 50% of ICF with the mean fatigue velocity of $0.182{\pm}0.006g/sec$($FV_{0/0.5}$, n=135) and from 50% to 25% of ICF with $0.084{\pm}0.004g/sec$($FV_{0.5/0.25}$, n=135). Cromakalim($50{\mu}M$) significantly increased $FV_{0.5/0.25}$(n=4). Glibenclamide($IC_{50}>50{\mu}M$), $Ba^{2+}$($IC_{50}=10{\mu}M$), 4-aminopyridine($FV_{0/0.5}$, $IC_{50}=0.5mM$; $FV_{0.5/0.25}$, $IC_{50}=2mM$) decreased both $FV_{0/0.5}$ and $FV_{0.5/0.25}$ concentration-dependently up to 75%. $TEA^+$(30mM), E-4031($10{\mu}M$), tolbutamide(1mM) decreased $FV_{0.5/0.25}$, but apamin(300nM) and $TEA^+$(10mM) showed no significant effects. Our results suggest that activation of the $K_{ATP}$ channels may be major cause of $K^+$ outflux during development of the fatigue and the isolated EHL muscle could be an useful experimental preparation in studying the fatigue phenomena in skeletal muscle. In addition, the possibility of activation of delayed rectifier during the fatigue development remains to be studied further.

• Proceedings of the Korean Biophysical Society Conference
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• 1996.07a
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• pp.35-35
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• 1996

Nitric oxide (NO) has been reported to have many roles in vivo ranging from the neurotransmitter in brain to the relaxant in smooth muscles. Recently, using inside-out patches, Bolotina et al. (1) showed that relaxing effect of NO is aortic smooth muscle is through direct activation of Ca2+-activated K+ channels (maxi-K), resulting in hyperpolarization. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.5
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• pp.215-219
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• 2007

Small and large conductance $Ca^{2+}$-activated $K^+(SK_{Ca}\;and\;BK_{Ca})$ channels are implicated in the modulation of neuronal excitability. We investigated how changes in peripheral $K_{Ca}$ channel activity affect mechanical sensitivity as well as the afferent fiber type responsible for $K_{Ca}$ channel-induced mechanical sensitivity. Blockade of $SK_{Ca}$ and $BK_{Ca}$ channels induced a sustained decrease of mechanical threshold which was significantly attenuated by topical application of capsaicin onto afferent fiber and intraplantar injection of 1-ethyl-2-benzimidazolinone. NS1619 selectively attenuated the decrease of mechanical threshold induced by charybdotoxin, but not by apamin. Spontaneous flinching and paw thickness were not significantly different after $K_{Ca}$ channel blockade. These results suggest that mechanical sensitivity can be modulated by $K_{Ca}$ channels on capsaicin-sensitive afferent fibers.