Voltage-dependent membrane ionic currents in lamprey striated muscle

1987 ◽  
Vol 18 (5) ◽  
pp. 445-451
Author(s):  
Sh. Derke ◽  
G. A. Nasledov
Keyword(s):  
Striated Muscle ◽  
Ionic Currents ◽  
Voltage Dependent ◽  
Membrane Ionic Currents

Ionic Currents Underlying Fast Action Potentials in the Obliquely Striated Muscle Cells of the Octopus Arm

2002 ◽  
Vol 88 (6) ◽  
pp. 3386-3397 ◽  
Author(s):  
Dan Rokni ◽  
Binyamin Hochner
Keyword(s):  
Time Constant ◽  
Action Potentials ◽  
Striated Muscle ◽  
Muscle Cells ◽  
Ionic Currents ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Activation Kinetics ◽  
Voltage Dependent ◽  
Neuromuscular Systems

The octopus arm provides a unique model for neuromuscular systems of flexible appendages. We previously reported the electrical compactness of the arm muscle cells and their rich excitable properties ranging from fast oscillations to overshooting action potentials. Here we characterize the voltage-activated ionic currents in the muscle cell membrane. We found three depolarization-activated ionic currents: 1) a high-voltage-activated L-type Ca2+ current, which began activating at approximately −35 mV, was eliminated when Ca2+ was substituted by Mg2+, was blocked by nifedipine, and showed Ca2+-dependent inactivation. This current had very rapid activation kinetics (peaked within milliseconds) and slow inactivation kinetics (τ in the order of 50 ms). 2) A delayed rectifier K+ current that was totally blocked by 10 mM TEA and partially blocked by 10 mM 4-aminopyridine (4AP). This current exhibited relatively slow activation kinetics (τ in the order of 15 ms) and inactivated only partially with a time constant of ∼150 ms. And 3) a transient A-type K+ current that was totally blocked by 10 mM 4AP and was partially blocked by 10 mM TEA. This current exhibited very fast activation kinetics (peaked within milliseconds) and inactivated with a time constant in the order of 60 ms. Inactivation of the A-type current was almost complete at −40 mV. No voltage-dependent Na+ current was found in these cells. The octopus arm muscle cells generate fast (∼3 ms) overshooting spikes in physiological conditions that are carried by a slowly inactivating L-type Ca2+ current.

scholarly journals High Capability of Pentagalloylglucose (PGG) in Inhibiting Multiple Types of Membrane Ionic Currents

2020 ◽  
Vol 21 (24) ◽  
pp. 9369
Author(s):  
Wei-Ting Chang ◽  
Ping-Yen Liu ◽  
Sheng-Nan Wu
Keyword(s):  
Ionic Currents ◽  
Gh3 Cells ◽  
Delayed Rectifier ◽  
Oxidative Property ◽  
Ic50 Value ◽  
Voltage Dependent ◽  
Ramp Voltage ◽  
Pentagalloyl Glucose ◽  
K Current ◽  
Membrane Ionic Currents

Pentagalloyglucose (PGG, penta-O-galloyl-β-d-glucose; 1,2,3,4,6-pentagalloyl glucose), a pentagallic acid ester of glucose, is recognized to possess anti-bacterial, anti-oxidative and anti-neoplastic activities. However, to what extent PGG or other polyphenolic compounds can perturb the magnitude and/or gating of different types of plasmalemmal ionic currents remains largely uncertain. In pituitary tumor (GH3) cells, we found out that PGG was effective at suppressing the density of delayed-rectifier K+ current (IK(DR)) concentration-dependently. The addition of PGG could suppress the density of proton-activated Cl− current (IPAC) observed in GH3 cells. The IC50 value required for the inhibitory action of PGG on IK(DR) or IPAC observed in GH3 cells was estimated to be 3.6 or 12.2 μM, respectively, while PGG (10 μM) mildly inhibited the density of the erg-mediated K+ current or voltage-gated Na+ current. The presence of neither chlorotoxin, hesperetin, kaempferol, morin nor iberiotoxin had any effects on IPAC density, whereas hydroxychloroquine or 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5yl)oxy] butanoic acid suppressed current density effectively. The application of PGG also led to a decrease in the area of voltage-dependent hysteresis of IPAC elicited by long-lasting isosceles-triangular ramp voltage command, suggesting that hysteretic strength was lessened in its presence. In human cardiac myocytes, the exposure to PGG also resulted in a reduction of ramp-induced IK(DR) density. Taken literally, PGG-perturbed adjustment of ionic currents could be direct and appears to be independent of its anti-oxidative property.

Altered Regulation of Potassium and Calcium Channels by GABAB and Adenosine Receptors in Hippocampal Neurons From Mice Lacking Gαo

2000 ◽  
Vol 83 (2) ◽  
pp. 1010-1018 ◽  
Author(s):  
Gabriela J. Greif ◽  
Deborah L. Sodickson ◽  
Bruce P. Bean ◽  
Eva J. Neer ◽  
Ulrike Mende
Keyword(s):  
Time Constant ◽  
Hippocampal Neurons ◽  
Ionic Currents ◽  
Absolute Requirement ◽  
Voltage Dependent ◽  
Hippocampal Ca3 ◽  
Ca3 Neurons ◽  
Inwardly Rectifying ◽  
G Protein Coupled

To examine the role of Go in modulation of ion channels by neurotransmitter receptors, we characterized modulation of ionic currents in hippocampal CA3 neurons from mice lacking both isoforms of Gαo. In CA3 neurons from Gαo −/− mice, 2-chloro-adenosine and the GABAB-receptor agonist baclofen activated inwardly rectifying K+ currents and inhibited voltage-dependent Ca2+ currents just as effectively as in Gαo +/+ littermates. However, the kinetics of transmitter action were dramatically altered in Gαo −/− mice in that recovery on washout of agonist was much slower. For example, recovery from 2-chloro-adenosine inhibition of calcium current was more than fourfold slower in neurons from Gαo −/− mice [time constant of 12.0 ± 0.8 (SE) s] than in neurons from Gαo +/+ mice (time constant of 2.6 ± 0.2 s). Recovery from baclofen effects was affected similarly. In neurons from control mice, effects of both baclofen and 2-chloro-adenosine on Ca2+ currents and K+currents were abolished by brief exposure to external N-ethyl-maleimide (NEM). In neurons lacking Gαo, some inhibition of Ca2+ currents by baclofen remained after NEM treatment, whereas baclofen activation of K+ currents and both effects of 2-chloro-adenosine were abolished. These results show that modulation of Ca2+ and K+ currents by G protein-coupled receptors in hippocampal neurons does not have an absolute requirement for Gαo. However, modulation is changed in the absence of Gαo in having much slower recovery kinetics. A likely possibility is that the very abundant Gαo is normally used but, when absent, can readily be replaced by G proteins with different properties.

scholarly journals Kinetic analysis of the action of Leiurus scorpion alpha-toxin on ionic currents in myelinated nerve.

1985 ◽  
Vol 86 (5) ◽  
pp. 739-762 ◽  
Author(s):  
G K Wang ◽  
G Strichartz
Keyword(s):  
Steady State ◽  
Ionic Currents ◽  
Na Channel ◽  
Dependent Manner ◽  
Na Current ◽  
Toxin Concentration ◽  
Toxin Molecule ◽  
Channel Inactivation ◽  
Na Currents ◽  
Voltage Dependent

The effects of a neurotoxin, purified from the venom of the scorpion Leiurus quinquestriatus, on the ionic currents of toad single myelinated fibers were studied under voltage-clamp conditions. Unlike previous investigations using crude scorpion venom, purified Leiurus toxin II alpha at high concentrations (200-400 nM) did not affect the K currents, nor did it reduce the peak Na current in the early stages of treatment. The activation of the Na channel was unaffected by the toxin, the activation time course remained unchanged, and the peak Na current vs. voltage relationship was not altered. In contrast, Na channel inactivation was considerably slowed and became incomplete. As a result, a steady state Na current was maintained during prolonged depolarizations of several seconds. These steady state Na currents had a different voltage dependence from peak Na currents and appeared to result from the opening of previously inactivated Na channels. The opening kinetics of the steady state current were exponential and had rates approximately 100-fold slower than the normal activation processes described for transitions from the resting state to the open state. In addition, the dependence of the peak Na current on the potential of preceding conditioning pulses was also dramatically altered by toxin treatment; this parameter reached a minimal value near a membrane potential of -50 mV and then increased continuously to a "plateau" value at potentials greater than +50 mV. The amplitude of this plateau was dependent on toxin concentration, reaching a maximum value equal to approximately 50% of the peak current; voltage-dependent reversal of the toxin's action limits the amplitude of the plateauing effect. The measured plateau effect was half-maximum at a toxin concentration of 12 nM, a value quite similar to the concentration producing half of the maximum slowing of Na channel inactivation. The results of Hill plots for these actions suggest that one toxin molecule binds to one Na channel. Thus, the binding of a single toxin molecule probably both produces the steady state currents and slows the Na channel inactivation. We propose that Leiurus toxin inhibits the conversion of the open state to inactivated states in a voltage-dependent manner, and thereby permits a fraction of the total Na permeability to remain at membrane potentials where inactivation is normally complete.

scholarly journals Characterization of Inhibitory Effectiveness in Hyperpolarization-Activated Cation Currents by a Group of ent-Kaurane-Type Diterpenoids from Croton tonkinensis

2020 ◽  
Vol 21 (4) ◽  
pp. 1268 ◽  
Author(s):  
Ping-Chung Kuo ◽  
Yen-Chin Liu ◽  
Yi-Ching Lo ◽  
Sheng-Nan Wu
Keyword(s):  
Ionic Currents ◽  
Neuroendocrine Cells ◽  
Flowering Plant ◽  
Gh3 Cells ◽  
Functional Activities ◽  
Cation Current ◽  
Voltage Dependent ◽  
K Current ◽  
The Common

Croton is an extensive flowering plant genus in the spurge family, Euphorbiaceae. Three croton compounds with the common ent-kaurane skeleton have been purified from Croton tonkinensis. Methods: We examined any modifications of croton components (i.e., croton-01 [ent-18-acetoxy-7α-hydroxykaur-16-en-15-one], croton-02 [ent-7α,14β-dihydroxykaur-16-en-15-one] and croton-03 [ent-1β-acetoxy-7α,14β-dihydroxykaur-16-en-15-one] on either hyperpolarization-activated cation current (Ih) or erg-mediated K+ current identified in pituitary tumor (GH3) cells and in rat insulin-secreting (INS-1) cells via patch-clamp methods. Results: Addition of croton-01, croton-02, or croton-03 effectively and differentially depressed Ih amplitude. Croton-03 (3 μM) shifted the activation curve of Ih to a more negative potential by approximately 11 mV. The voltage-dependent hysteresis of Ih was also diminished by croton-03 administration. Croton-03-induced depression of Ih could not be attenuated by SQ-22536 (10 μM), an inhibitor of adenylate cyclase, but indeed reversed by oxaliplatin (10 μM). The Ih in INS-1 cells was also depressed effectively by croton-03. Conclusion: Our study highlights the evidence that these ent-kaurane diterpenoids might conceivably perturb these ionic currents through which they have high influence on the functional activities of endocrine or neuroendocrine cells.

Excitability Increase Induced by β-Adrenergic Receptor-Mediated Activation of Hyperpolarization-Activated Cation Channels in Rat Cerebellar Basket Cells

2000 ◽  
Vol 84 (4) ◽  
pp. 2026-2034 ◽  
Author(s):  
Fumihito Saitow ◽  
Shiro Konishi
Keyword(s):  
Preceding Paper ◽  
Input Resistance ◽  
Ionic Currents ◽  
Synaptic Activity ◽  
Basket Cells ◽  
Camp Analogue ◽  
Voltage Dependent ◽  
Current Clamp Mode ◽  
Old Rats ◽  
Whole Cell Recordings

In the preceding paper, we showed that norepinephrine (NE) enhances the spontaneous spike firings in cerebellar interneurons, basket cells (BCs), resulting in an increase in the frequency of BC-spike-triggered inhibitory postsynaptic currents (IPSCs) in Purkinje cells (PCs), and that the effects of NE on GABAergic BCs are mediated by β2-adrenergic receptors. This study aimed to further examine the ionic mechanism underlying the β-adrenoceptor-mediated facilitation of GABAergic transmission at the BC-PC synapses. Using cerebellar slices obtained from 15- to 21-day-old rats and whole cell recordings, we investigated ionic currents in the BCs and the effects of the β-agonist isoproterenol (ISP) as well as forskolin on the BC excitability. Hyperpolarizing voltage steps from a holding potential of −50 mV elicited a hyperpolarization-activated inward current, I h, in the BC. This current exhibited voltage-dependent activation that was accelerated by strong hyperpolarization, displaying two time constants, 84 ± 6 and 310 ± 40 ms, at −100 mV, and was inhibited by 20 μM ZD7288. ISP and forskolin, both at 20 μM, enhanced I h by shifting the activation curve by 5.9 and 9.3 mV toward positive voltages, respectively. Under the current-clamp mode, ISP produced a depolarization of 7 ± 3 mV in BCs and reduced their input resistance to 74 ± 6%. ISP and a cAMP analogue, Rp-cAMP-S, increased the frequency of spontaneous spikes recorded from BCs using the cell-attached mode. The I h inhibitor ZD7288 decreased the BC spike frequency and abolished the ISP-induced increase in spike discharges. The results suggest that NE depolarizes the BCs through β-adrenoceptor-mediated cAMP formation linking it to activation of I h, which is, at least in part, involved in noradrenergic afferent-mediated facilitation of GABAergic synaptic activity at BC-PC connections in the rat cerebellum.

scholarly journals NIK-247 Blocks Voltage-Dependent Ionic Currents in Crayfish Axon

1991 ◽  
Vol 57 (4) ◽  
pp. 545-552
Author(s):  
Jun Kojima ◽  
Yoshiko Sugawara ◽  
Shosaku Obara
Keyword(s):  
Ionic Currents ◽  
Voltage Dependent

Effects of melatonin on ionic currents in cultured ocular tissues

1999 ◽  
Vol 276 (4) ◽  
pp. C923-C929 ◽  
Author(s):  
Adam Rich ◽  
Gianrico Farrugia ◽  
James L. Rae
Keyword(s):  
Epithelial Cells ◽  
Trabecular Meshwork ◽  
Cell Voltage ◽  
Ionic Currents ◽  
Lens Epithelial Cells ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Epithelial Cell Line ◽  
Voltage Dependent ◽  
Mouse Lens

The effects of melatonin on ionic conductances in a cultured mouse lens epithelial cell line (α-TN4) and in cultured human trabecular meshwork (HTM) cells were measured using the amphotericin perforated patch whole cell voltage-clamp technique. Melatonin stimulated a voltage-dependent Na+-selective current in lens epithelial cells and trabecular meshwork cells. The effects of melatonin were observed at 50 pM and were maximal at 100 μM. Melatonin enhanced activation and inactivation kinetics, but no change was observed in the voltage dependence of activation. The results are consistent with an increase in the total number of ion channels available for activation by membrane depolarization. Melatonin was also found to stimulate a K+-selective current at high doses (1 mM). Melatonin did not affect the inwardly rectifying K+ current or the delayed rectifier type K+ current that has been described in cultured mouse lens epithelial cells. The results show that melatonin specifically stimulated the TTX-insensitive voltage-dependent Na+ current by an apparently novel mechanism.

scholarly journals Numerical Simulations of Fractionated Electrograms and Pathological Cardiac Action Potential

2002 ◽  
Vol 4 (3) ◽  
pp. 167-181 ◽  
Author(s):  
Simona Sanfelici
Keyword(s):  
Numerical Simulations ◽  
Cardiac Tissue ◽  
Time Discretization ◽  
Ionic Currents ◽  
Bidomain Model ◽  
Approximation Process ◽  
Point Of Interest ◽  
Intracellular Conductivity ◽  
Membrane Ionic Currents ◽  
Fractionated Electrograms

The aim of this work is twofold. First we focus on the complex phenomenon of electrogram fractionation, due to the presence of discontinuities in the conduction properties of the cardiac tissue in a bidomain model. Numerical simulations of paced activation may help to understand the role of the membrane ionic currents and of the changes in cellular coupling in the formation of conduction blocks and fractionation of the electrogram waveform. In particular, we show that fractionation is independent ofINAalterations and that it can be described by the bidomain model of cardiac tissue. Moreover, some deflections in fractionated electrograms may give nonlocal information about the shape of damaged areas, also revealing the presence of inhomogeneities in the intracellular conductivity of the medium at a distance.The second point of interest is the analysis of the effects of space–time discretization on numerical results, especially during slow conduction in damaged cardiac tissue. Indeed, large discretization steps can induce numerical artifacts such as slowing down of conduction velocity, alteration in extracellular and transmembrane potential waveforms or conduction blocks, which are not predicted by the continuous bidomain model. Several possible numerical and physiological explanations of these effects are given. Essentially, the discrete system obtained at the end of the approximation process may be interpreted as a discrete model of the cardiac tissue made up of isopotential cells where the effective intracellular conductivity tensor depends on the space discretization steps; the increase of these steps results in an increase of the effective intracellular resistance and can induce conduction blocks if a certain critical value is exceeded.

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