No abstract available.
Latex* ; Polystyrenes* ; Potassium Channels* ; Potassium* ; Vasospasm, Intracranial*

Potassium-selective channels are the largest and most diverse group of ion channels in the human. Also, potassium-selective channels are important in many cells during anesthesia. Many researches have focused on potassium channel and intravenous anesthetics.
Anesthesia ; Anesthetics, Intravenous ; Humans ; Ion Channels ; Potassium Channels

OBJECTS:We investigated a possible association between the polymorphic trinucleotide repeat(TNR) expansion in neuronal potassium channel gene KCNN3 and schizophrenia. METHODS: CAG/CTG repeat distribution in KCNN3, CTG18.1 and ERDA1 was examined and the copy number of ligation product in repeat expansion detection(RED) was measured in Korean patients with schizophrenia(n=245) and ethnically matched healthy controls(n=116). RESULTS: Longer alleles in the KCNN3 gene were over-represented in patients. The frequency of alleles with CAG repeats longer than 19 copy in the KCNN3 gene was higher in the patients with schizophrenia as compared to controls(73.3% vs. 65.1%;p=0.029, Fisher's exact test). And this difference was more prominent in schizophrenic patients with familial background(p=0.03, Fisher's exact test). We found no difference in the frequency of longer alleles between negative and positive subtypes of schizophrenia. Ligation product size in RED and alleles with CAG repeat number in the CTG18.1 gene was not increased in the patients. The copy number of ligation product in RED was highly correlated with CAG/CTG copies of ERDA1 in the patient group(r=0.45, p<0.001) as well as in the control group(r=0.44, p<0.001). However, CAG repeat length in the KCNN3 gene was not correlated with ERDA1 score. CONCLUSIONS: Our results support the hypothesis that the longer allele of KCNN3 may be considered as a candidate gene for schizophrenia, especially in the case with familial background. And the RED assay results was affected by the CAG copy number of ERDA1.
Alleles ; Humans ; Ligation ; Neurons ; Potassium Channels ; Schizophrenia*

Arrhythmias, Cardiac ; Humans ; Large-Conductance Calcium-Activated Potassium Channels ; Small-Conductance Calcium-Activated Potassium Channels

The intermediate conductance Ca2+-activated K+ channels (SK4, IKCa1) are present in lymphocytes, and their membrane expression is upregulated by various immunological stimuli. In this study, the activity of SK4 was compared between Bal-17 and WEHI-231 cell lines which represent mature and immature stages of murine B lymphocytes, respectively. The whole-cell patch clamp with high-Ca2+ (0.8microM) KCl pipette solution revealed a voltage-independent K+ current that was blocked by clotrimazole (1 mM), an SK4 blocker. The expression of mRNAs for SK4 was confirmed in both Bal-17 and WEHI-231 cells. The density of clotrimazole-sensitive SK4 current was significantly larger in Bal-17 than WEHI-231 cells (-11.4+/-3.1 Vs. -5.7+/-1.15 pA/pF). Also, the chronic stimulation of B cell receptors (BCR) by BCR-ligation (anti-IgM Ab, 3microgram/ml, 8~12 h) significantly upregulated the amplitude of clotrimazole-sensitive current from -11.4+/-3.1 to -53.1+/-8.6 pA/pF in Bal-17 cells. In WEHI-231 cells, the effect of BCR-ligation was significantly small (-5.7+/-1.15 to -9.0+/-1.00 pA/pF). The differential expression and regulation by BCR-ligation might reflect functional changes in the maturation of B lymphocytes.
B-Lymphocytes* ; Cell Line ; Clotrimazole ; Lymphocytes ; Membranes ; Potassium Channels ; Potassium Channels, Calcium-Activated ; RNA, Messenger

Ischemic damage is one of the most serious problems. The openers of KATP channel have been suggested to have an effect to limit the ischemic damage. However, it is not yet clear how KATP channels of a cell correspond to hypoxic damage. To address the question, N2a cells were exposed to two different hypoxic conditions as follows: 6 hours hypoxia followed by 3 hours reperfusion and 12 hours hypoxia followed by 3 hours reperfusion. As the results, 6 hours hypoxic treatment increased glibenclamide-sensitive basal KATP current activity (approximately 6.5-fold at 0 mV test potential) when compared with nomoxic condition. In contrast, 12 hours hypoxic treatment induced a relatively smaller change in the KATP current density (2.5-fold at 0 mV test potential). Additionally, in experiments where KATP channels were opened using diazoxide, the hypoxia for 6 hours significantly increased the current density in comparison to control condition (p < 0.001). Interestingly, the augmentation in the KATP current density reduced after exposure to the 12 hours hypoxic condition (p < 0.001). Taken together, these results suggest that KATP channels appear to be recruited more in cells exposed to the 6 hours hypoxic condition and they may play a protective role against hypoxia-reperfusion damage within the time range.
Animals ; Anoxia ; Diazoxide ; Glyburide ; KATP Channels ; Mice* ; Neuroblastoma* ; Potassium Channels* ; Potassium* ; Reperfusion

Renal outer medullary potassium (ROMK) channel is an important K⁺ excretion channel in the body, and K⁺ secreted by the ROMK channels is most or all source of urinary potassium. Previous studies focused on the ROMK channels of thick ascending limb (TAL) and collecting duct (CD), while there were few studies on the involvement of ROMK channels of the late distal convoluted tubule (DCT2) in K⁺ excretion. The purpose of the present study was mainly to record the ROMK channels current in renal DCT2 and observe the effect of high potassium diet on the ROMK channels by using single channel and whole-cell patch-clamp techniques. The results showed that a small conductance channel current with a conductance of 39 pS could be recorded in the apical membrane of renal DCT2, and it could be blocked by Tertiapin-Q (TPNQ), a ROMK channel inhibitor. The high potassium diet significantly increased the probability of ROMK channel current occurrence in the apical membrane of renal DCT2, and enhanced the activity of ROMK channel, compared to normal potassium diet (P < 0.01). Western blot results also demonstrated that the high potassium diet significantly up-regulated the protein expression levels of ROMK channels and epithelial sodium channel (ENaC), and down-regulated the protein expression level of Na⁺-Cl^- cotransporter (NCC). Moreover, the high potassium diet significantly increased urinary potassium excretion. These results suggest that the high potassium diet may activate the ROMK channels in the apical membrane of renal DCT2 and increase the urinary potassium excretion by up-regulating the expression of renal ROMK channels.
Potassium Channels, Inwardly Rectifying/metabolism* ; Kidney Tubules, Distal/metabolism* ; Potassium/metabolism* ; Epithelial Sodium Channels/metabolism* ; Diet

PURPOSE: This study was performed to determine the effects of phytoestrogen on seminal vesicle excitability. MATERIALS AND METHODS: Single smooth muscle cells of seminal vesicle were obtained from rabbits using proteolytic enzymes(collagenase). Using single cell and channel recording methods of patch clamp, the various currents of potassium channels in smooth muscle cells were recorded. Potassium currents were divided into calcium dependent and independent. RESULTS: Most of the calcium dependent K currents were maxi-K currents and most of calcium independent ones were delayed rectifier K currents. Inside-out patch clamp technique was used to characterize the maxi-K channel. The channel showed outward rectification and calcium dependency. The single-channel conductance of this channel estimated from slope conductance was 119.4+/-11.7 pS under physiological conditions. These characteristics were typical properties of maxi-K channels. Application of genistein(10micronM) rarely affected the delayed rectifier K channel activities, but it evoked significant increase of maxi-K channel activities at both single cell and channel levels. CONCLUSIONS: From these results it is strongly suggested that the excitability and contractility of seminal vesicle might be modulated by genistein through a mechanism of maxi-K channel activation.
Calcium ; Genistein ; Large-Conductance Calcium-Activated Potassium Channels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Phytoestrogens* ; Potassium Channels* ; Potassium* ; Rabbits ; Seminal Vesicles*

We performed experiments using Aplysia neurons to identify the mechanism underlying the changes in the firing patterns in response to temperature changes. When the temperature was gradually increased from 11degrees C to 31degrees C the firing patterns changed sequentially from the silent state to beating, doublets, beating-chaos, bursting-chaos, square-wave bursting, and bursting-oscillation patterns. When the temperature was decreased over the same temperature range, these sequential changes in the firing patterns reappeared in reverse order. To simulate this entire range of spiking patterns we modified nonlinear differential equations that Chay and Lee made using temperature-dependent scaling factors. To refine the equations, we also analyzed the spike pattern changes in the presence of potassium channel blockers. Based on the solutions of these equations and potassium channel blocker experiments, we found that, as temperature increases, the maximum value of the potassium channel relaxation time constant, taun(t) increases, but the maximum value of the probabilities of openings for activation of the potassium channels, n(t) decreases. Accordingly, the voltage-dependent potassium current is likely to play a leading role in the temperature-dependent changes in the firing patterns in Aplysia neurons.
Aplysia ; Computer Simulation ; Fires ; Neurons ; Potassium ; Potassium Channel Blockers ; Potassium Channels ; Relaxation

PURPOSE: Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant channelopathy characterized by episodic attacks of muscle weakness and hypokalemia. Mutations in the calcium channel gene, CACNA1S, or the sodium channel gene, SCN4A, have been found to be responsible for HOKPP; however, the mechanism that causes hypokalemia remains to be determined. The aim of this study was to improve the understanding of this mechanism by investigating the expression of calcium-activated potassium (KCa) channel genes in HOKPP patients. METHODS: We measured the intracellular calcium concentration with fura-2-acetoxymethyl ester in skeletal muscle cells of HOKPP patients and healthy individuals. We examined the mRNA and protein expression of KCa channel genes (KCNMA1, KCNN1, KCNN2, KCNN3, and KCNN4) in both cell types. RESULTS: Patient cells exhibited higher cytosolic calcium levels than normal cells. Quantitative reverse transcription polymerase chain reaction analysis showed that the mRNA levels of the KCa channel genes did not significantly differ between patient and normal cells. However, western blot analysis showed that protein levels of the KCNMA1 gene, which encodes KCa1.1 channels (also called big potassium channels), were significantly lower in the membrane fraction and higher in the cytosolic fraction of patient cells than normal cells. When patient cells were exposed to 50 mM potassium buffer, which was used to induce depolarization, the altered subcellular distribution of BK channels remained unchanged. CONCLUSION: These findings suggest a novel mechanism for the development of hypokalemia and paralysis in HOKPP and demonstrate a connection between disease-associated mutations in calcium/sodium channels and pathogenic changes in nonmutant potassium channels.
Blotting, Western ; Calcium ; Calcium Channels ; Channelopathies ; Cytosol ; Humans ; Hypokalemia ; Hypokalemic Periodic Paralysis* ; Large-Conductance Calcium-Activated Potassium Channels ; Membranes ; Muscle Weakness ; Muscle, Skeletal ; Paralysis ; Polymerase Chain Reaction ; Potassium ; Potassium Channels ; Potassium Channels, Calcium-Activated* ; Reverse Transcription ; RNA, Messenger ; Sodium Channels