• Title/Summary/Keyword: Sub-channels

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Electrophysiological Properties of Ion Channels in Ascaris suum Tissue Incorporated into Planar Lipid Bilayers

  • Park, Kwon Moo;Kim, Sun-Don;Park, Jin Bong;Hong, Sung-Jong;Ryu, Pan Dong
    • Parasites, Hosts and Diseases
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    • v.59 no.4
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    • pp.329-339
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    • 2021
  • Ion channels are important targets of anthelmintic agents. In this study, we identified 3 types of ion channels in Ascaris suum tissue incorporated into planar lipid bilayers using an electrophysiological technique. The most frequent channel was a large-conductance cation channel (209 pS), which accounted for 64.5% of channels incorporated (n=60). Its open-state probability (Po) was ~0.3 in the voltage range of -60~+60 mV. A substate was observed at 55% of the main-state. The permeability ratio of Cl- to K+ (PCl/PK) was ~0.5 and PNa/PK was 0.81 in both states. Another type of cation channel was recorded in 7.5% of channels incorporated (n=7) and discriminated from the large-conductance cation channel by its smaller conductance (55.3 pS). Its Po was low at all voltages tested (~0.1). The third type was an anion channel recorded in 27.9% of channels incorporated (n=26). Its conductance was 39.0 pS and PCl/PK was 8.6±0.8. Po was ~1.0 at all tested potentials. In summary, we identified 2 types of cation and 1 type of anion channels in Ascaris suum. Gating of these channels did not much vary with voltage and their ionic selectivity is rather low. Their molecular nature, functions, and potentials as anthelmintic drug targets remain to be studied further.

Consensus channelome of dinoflagellates revealed by transcriptomic analysis sheds light on their physiology

  • Pozdnyakov, Ilya;Matantseva, Olga;Skarlato, Sergei
    • ALGAE
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    • v.36 no.4
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    • pp.315-326
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    • 2021
  • Ion channels are membrane protein complexes mediating passive ion flux across the cell membranes. Every organism has a certain set of ion channels that define its physiology. Dinoflagellates are ecologically important microorganisms characterized by effective physiological adaptability, which backs up their massive proliferations that often result in harmful blooms (red tides). In this study, we used a bioinformatics approach to identify homologs of known ion channels that belong to 36 ion channel families. We demonstrated that the versatility of the dinoflagellate physiology is underpinned by a high diversity of ion channels including homologs of animal and plant proteins, as well as channels unique to protists. The analysis of 27 transcriptomes allowed reconstructing a consensus ion channel repertoire (channelome) of dinoflagellates including the members of 31 ion channel families: inwardly-rectifying potassium channels, two-pore domain potassium channels, voltage-gated potassium channels (Kv), tandem Kv, cyclic nucleotide-binding domain-containing channels (CNBD), tandem CNBD, eukaryotic ionotropic glutamate receptors, large-conductance calcium-activated potassium channels, intermediate/small-conductance calcium-activated potassium channels, eukaryotic single-domain voltage-gated cation channels, transient receptor potential channels, two-pore domain calcium channels, four-domain voltage-gated cation channels, cation and anion Cys-loop receptors, small-conductivity mechanosensitive channels, large-conductivity mechanosensitive channels, voltage-gated proton channels, inositole-1,4,5-trisphosphate receptors, slow anion channels, aluminum-activated malate transporters and quick anion channels, mitochondrial calcium uniporters, voltage-dependent anion channels, vesicular chloride channels, ionotropic purinergic receptors, animal volage-insensitive cation channels, channelrhodopsins, bestrophins, voltage-gated chloride channels H+/Cl- exchangers, plant calcium-permeable mechanosensitive channels, and trimeric intracellular cation channels. Overall, dinoflagellates represent cells able to respond to physical and chemical stimuli utilizing a wide range of G-protein coupled receptors- and Ca2+-dependent signaling pathways. The applied approach not only shed light on the ion channel set in dinoflagellates, but also provided the information on possible molecular mechanisms underlying vital cellular processes dependent on the ion transport.

Modification of Insect Sodium Currents by a Pyrethroid Permethrin and Positive Cooperativity with Scorpion Toxins (피레스로이드계 살충제 퍼메트린이 Heliothis virescens 중추신경세포에 있는 나트륨채널에 작용하는 기작을 전기생리학적으로 연구)

  • Lee, Daewoo;Adams, Michael E.
    • Korean journal of applied entomology
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    • v.61 no.1
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    • pp.117-128
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    • 2022
  • In this study, we have examined pyrethroid actions on sodium channels in the pest insect Heliothis virescens. The synthetic pyrethroid permethrin increased steady-state sodium current in H. virescens central neurons and prolonged tail currents (INa-tail) due to extreme slowing of sodium channel deactivation. Prolongation of INa-tail was evident at permethrin concentrations as low as 60 nM, which modified ~1.7% of sodium channels and 10 μM permethrin modified about 30% of channels. The average time constant (τ1) of tail current decay was ~335 ms for permethrin-modified channels. These modified channels activated at more negative potentials and showed slower activation kinetics, and failed to inactivate. Permethrin modification of sodium channels was dramatically potentiated by the α scorpion toxin LqhαIT, showing positive cooperativity between two binding sites. The amplitude of the tail current induced by 0.3 μM permethrin was enhanced ~8-fold by LqhαIT (200 pM). Positive cooperativity was also observed between permethrin and the insect-specific scorpion toxin AaIT as 10 nM permethrin potentiated the shift of voltage dependence caused by AaIT (~2-fold).

Ethanol inhibits Kv7.2/7.3 channel open probability by reducing the PI(4,5)P2 sensitivity of Kv7.2 subunit

  • Kim, Kwon-Woo;Suh, Byung-Chang
    • BMB Reports
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    • v.54 no.6
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    • pp.311-316
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    • 2021
  • Ethanol often causes critical health problems by altering the neuronal activities of the central and peripheral nerve systems. One of the cellular targets of ethanol is the plasma membrane proteins including ion channels and receptors. Recently, we reported that ethanol elevates membrane excitability in sympathetic neurons by inhibiting Kv7.2/7.3 channels in a cell type-specific manner. Even though our studies revealed that the inhibitory effects of ethanol on the Kv7.2/7.3 channel was diminished by the increase of plasma membrane phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), the molecular mechanism of ethanol on Kv7.2/7.3 channel inhibition remains unclear. By investigating the kinetics of Kv7.2/7.3 current in high K+ solution, we found that ethanol inhibited Kv7.2/7.3 channels through a mechanism distinct from that of tetraethylammonium (TEA) which enters into the pore and blocks the gate of the channels. Using a non-stationary noise analysis (NSNA), we demonstrated that the inhibitory effect of ethanol is the result of reduction of open probability (PO) of the Kv7.2/7.3 channel, but not of a single channel current (i) or channel number (N). Finally, ethanol selectively facilitated the kinetics of Kv7.2 current suppression by voltage-sensing phosphatase (VSP)-induced PI(4,5)P2 depletion, while it slowed down Kv7.2 current recovery from the VSP-induced inhibition. Together our results suggest that ethanol regulates neuronal activity through the reduction of open probability and PI(4,5)P2 sensitivity of Kv7.2/7.3 channels.

Negative self-regulation of transient receptor potential canonical 4 by the specific interaction with phospholipase C-δ1

  • Juyeon Ko;Jinhyeong Kim;Jongyun Myeong;Misun Kwak;Insuk So
    • The Korean Journal of Physiology and Pharmacology
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    • v.27 no.2
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    • pp.187-196
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    • 2023
  • Transient receptor potential canonical (TRPC) channels are non-selective calcium-permeable cation channels. It is suggested that TRPC4β is regulated by phospholipase C (PLC) signaling and is especially maintained by phosphatidylinositol 4,5-bisphosphate (PIP2). In this study, we present the regulation mechanism of the TRPC4 channel with PIP2 hydrolysis which is mediated by a channel-bound PLCδ1 but not by the GqPCR signaling pathway. Our electrophysiological recordings demonstrate that the Ca2+ via an open TRPC4 channel activates PLCδ1 in the physiological range, and it causes the decrease of current amplitude. The existence of PLCδ1 accelerated PIP2 depletion when the channel was activated by an agonist. Interestingly, PLCδ1 mutants which have lost the ability to regulate PIP2 level failed to reduce the TRPC4 current amplitude. Our results demonstrate that TRPC4 self-regulates its activity by allowing Ca2+ ions into the cell and promoting the PIP2 hydrolyzing activity of PLCδ1.

A Study on the MC-CDMA Using CMFB IIR Filter

  • Shin, Jonghong;Jang, Sunbong;Jee, InnHo
    • Proceedings of the IEEK Conference
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    • 2002.07a
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    • pp.405-408
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    • 2002
  • Because of superior division among sub-channels, DWT MC-CDMA is less interference with neighborhood channel. In our newly proposed multi-carrier CDMA data transmission method, lIR CMFB filter banks sharply divide sub-bands and reduces spectral overlaps among neighboring sub-channels. In experiment result, proposed filter is better ability of sub-band division than FIR filter. Since the proposed cosine modulated filter banks lIR filter having wavelet property is designed to response sharp transition band, the ISI and ICI between neighboring sub-channels can be effectively reduced. And robustness about narrow band interference of CMFB IIR MC-CDMA almost same FIR DWT MC-CDMA.

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Analysis of the performances of random access channels in multi-service multi-user OFDMA systems according to resource management schemes (다중 서비스 다중 사용자 OFDMA 시스템에서의 자원할당방식에 따른 임의접근 채널 성능 분석)

  • Koo, In-Soo;Lee, Young-Du
    • Proceedings of the KIEE Conference
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    • 2007.04a
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    • pp.237-239
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    • 2007
  • In the paper, we analyze the performances of random access channels in multi-service multi-user OFDMA systems. The resource of the random access channels in OFDMA systems is the nubmer of available sub-channels and PN-codes. For given available sub-channels and PN-codes. we analyze the performances of the random access channels of OFDMA systems according to three resource allocation methods (resource full sharing, resource partial sharing, resource partition) in tenus of the access success probability, the blocking probability, the access delay and the throughput of each service class. Further, we find the feasible region of the access probability of each service class in which the allowable minimum access success probability, the allowable maximum blocking probability and the allowable maximum access delay are satisfied. The results also can be utilized to find proper region of the access probabilities of each service class for differentiated quality of service(QoS)s, and for the system operations.

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Security performance analysis of SIMO relay systems over Composite Fading Channels

  • Sun, Jiangfeng;Bie, Hongxia;Li, Xingwang
    • KSII Transactions on Internet and Information Systems (TIIS)
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    • v.14 no.6
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    • pp.2649-2669
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    • 2020
  • In this paper, we analyze the secrecy performance of single-input multiple-output (SIMO) relay systems over κ-μ shadowed fading channels. Based on considering relay model employing decode-and-forward (DF) protocol, two security evaluation metrics, namely, secure outage probability (SOP) and probability of strictly positive secrecy capacity (SPSC) are studied, for which closed-form analytical expressions are derived. In addition, Monte Carlo results prove the validity of the theoretical derivation. The simulation results confirm that the factors that enhance the security include large ratio of (μD, μE), (mD, mE), (LD, LE) and small ratio of (kD, kE) under the high signal-to-noise ratio regime.

Open channel block of Kv1.4 potassium channels by aripiprazole

  • Park, Jeaneun;Cho, Kwang-Hyun;Lee, Hong Joon;Choi, Jin-Sung;Rhie, Duck-Joo
    • 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.

Antiarrhythmic Effect of Artemisinin in an Ex-vivo Model of Brugada Syndrome Induced by NS5806

  • Hyung Ki Jeong;Seo Na Hong;Namsik Yoon;Ki Hong Lee;Hyung Wook Park;Jeong Gwan Cho
    • Korean Circulation Journal
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    • v.53 no.4
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    • pp.239-250
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    • 2023
  • Background and Objectives: Brugada syndrome (BrS) is an inherited arrhythmia syndrome that presents as sudden cardiac death (SCD) without structural heart disease. One of the mechanisms of SCD has been suggested to be related to the uneven dispersion of transient outward potassium current (Ito) channels between the epicardium and endocardium, thus inducing ventricular tachyarrhythmia. Artemisinin is widely used as an antimalarial drug. Its antiarrhythmic effect, which includes suppression of Ito channels, has been previously reported. We investigated the effect of artemisinin on the suppression of electrocardiographic manifestations in a canine experimental model of BrS. Methods: Transmural pseudo-electrocardiograms and epicardial/endocardial transmembrane action potentials (APs) were recorded from coronary-perfused canine right ventricular wedge preparations (n=8). To mimic the BrS phenotypes, acetylcholine (3 μM), calcium channel blocker verapamil (1 μM), and Ito agonist NS5806 (6-10 μM) were used. Artemisinin (100-150 μM) was then perfused to ameliorate the ventricular tachyarrhythmia in the BrS models. Results: The provocation agents induced prominent J waves in all the models on the pseudo-electrocardiograms. The epicardial AP dome was attenuated. Ventricular tachyarrhythmia was induced in six out of 8 preparations. Artemisinin suppressed ventricular tachyarrhythmia in all 6 of these preparations and recovered the AP dome of the right ventricular epicardium in all preparations (n=8). J wave areas and epicardial notch indexes were also significantly decreased after artemisinin perfusion. Conclusions: Our findings suggest that artemisinin has an antiarrhythmic effect on wedge preparation models of BrS. It might work by inhibition of potassium channels including Ito channels, subsequently suppressing ventricular tachycardia/ventricular fibrillation.