scholarly journals Barium-induced nondriven action potentials as a model of triggered potentials from early afterdepolarization: Significance of slow channel activity and differeing effects of quinidine and amiodarone

1990 ◽  
Vol 15 (1) ◽  
pp. 213-221 ◽  
Author(s):  
Chiei Takanaka ◽  
Bramah N. Singh
Keyword(s):  
Action Potentials ◽  
Channel Activity ◽  
Slow Channel ◽  
Early Afterdepolarization

scholarly journals Facilitation by hERG Channel Blockers Suppresses Early Afterdepolarization of Simulated Cardiac Action Potentials

2018 ◽  
Vol 114 (3) ◽  
pp. 474a
Author(s):  
Kazuharu Furutani ◽  
Kunichika Tsumoto ◽  
Jon T. Sack ◽  
Yoshihisa Kurachi
Keyword(s):  
Action Potentials ◽  
Herg Channel ◽  
Channel Blockers ◽  
Cardiac Action ◽  
Early Afterdepolarization

Participation of slow inward current in the Purkinje fiber action potential overshoot

1979 ◽  
Vol 237 (2) ◽  
pp. H204-H212
Author(s):  
L. Mary-Rabine ◽  
B. F. Hoffman ◽  
M. R. Rosen
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Inward Current ◽  
Slow Channel ◽  
Phase 0 ◽  
Relationship Of ◽  
The Relationship ◽  
Diastolic Potential

We used microelectrode techniques to study the relationship of canine Purkinje fiber membrane potential and the action potential (AP) overshoot. At the maximum diastolic potential, -93.0 +/- 0.5 (SE) mV, AP overshoot was +37.7 +/- 0.4 mV. There was a range of membrane potentials (MP) less negative than the maximum diastolic potential from which action potentials were elicited with an overshoot greater than the control. Starting at an MP of less than -78.7 +/- 0.4 mV, AP overshoot was less than control. A maximum overshoot of +40.2 +/- 0.4 mV occurred at an MP of -85.4 +/- 0.4 mV. The relationship of the maximum upstroke velocity (Vmax) of phase 0 depolarization to MP was sigmoidal. Peak Vmax, 497 +/- 13 V/s, occurred at MP greater than or equal to -89.3 +/- 0.5 mV. The increase in overshoot was enhanced as perfusate [Ca2+] increased and decreased as [Ca2+] decreased. Slow-channel blocking agents and tetrodotoxin (TTX) depressed the peak of the curve relating overshoot to MP. TTX also decreased Vmax. The effect of TTX on overshoot but not on Vmax was reversed with Ca2+, 8.1 mM. The increase in overshoot for action potentials initiated during the terminal part of phase 3 was due to a slow, delayed component of the upstroke and appears to result from the slow inward current.

scholarly journals Photochemical reaction cycle transitions during anion channelrhodopsin gating

2016 ◽  
Vol 113 (14) ◽  
pp. E1993-E2000 ◽  
Author(s):  
Oleg A. Sineshchekov ◽  
Hai Li ◽  
Elena G. Govorunova ◽  
John L. Spudich
Keyword(s):  
Schiff Base ◽  
Hek293 Cells ◽  
Proton Acceptor ◽  
Channel Activity ◽  
Wild Type ◽  
Anion Selectivity ◽  
Slow Channel ◽  
Guillardia Theta ◽  
Report Analysis ◽  
Ion Conducting

A recently discovered family of natural anion channelrhodopsins (ACRs) have the highest conductance among channelrhodopsins and exhibit exclusive anion selectivity, which make them efficient inhibitory tools for optogenetics. We report analysis of flash-induced absorption changes in purified wild-type and mutant ACRs, and of photocurrents they generate in HEK293 cells. Contrary to cation channelrhodopsins (CCRs), the ion conducting state of ACRs develops in an L-like intermediate that precedes the deprotonation of the retinylidene Schiff base (i.e., formation of an M intermediate). Channel closing involves two mechanisms leading to depletion of the conducting L-like state: (i) Fast closing is caused by a reversible L⇔M conversion. Glu-68 in Guillardia theta ACR1 plays an important role in this transition, likely serving as a counterion and proton acceptor at least at high and neutral pH. Incomplete suppression of M formation in the GtACR1_E68Q mutant indicates the existence of an alternative proton acceptor. (ii) Slow closing of the channel parallels irreversible depletion of the M-like and, hence, L-like state. Mutation of Cys-102 that strongly affected slow channel closing slowed the photocycle to the same extent. The L and M intermediates were in equilibrium in C102A as in the WT. In the position of Glu-123 in channelrhodopsin-2, ACRs contain a noncarboxylate residue, the mutation of which to Glu produced early Schiff base proton transfer and strongly inhibited channel activity. The data reveal fundamental differences between natural ACR and CCR conductance mechanisms and their underlying photochemistry, further confirming that these proteins form distinct families of rhodopsin channels.

ATP promotes development of afterdepolarizations and triggered activity in cardiac myocytes

1994 ◽  
Vol 267 (5) ◽  
pp. H2005-H2011 ◽  
Author(s):  
Y. Song ◽  
L. Belardinelli
Keyword(s):  
Action Potentials ◽  
Ventricular Myocytes ◽  
Extracellular Atp ◽  
Extracellular Medium ◽  
Triggered Activity ◽  
Arrhythmogenic Effect ◽  
Early Afterdepolarization ◽  
Triggered Arrhythmias ◽  
Delayed Afterdepolarization ◽  
Isolated Ventricular Myocytes

The effect of extracellular ATP on transient inward current (Iti), delayed afterdepolarization (DAD), early afterdepolarization (EAD), and triggered activity were investigated in guinea pig isolated ventricular myocytes. ATP alone did not induce afterdepolarizations nor did it significantly alter the resting membrane potentials and action potentials. However, when it was applied with drugs known to increase intracellular Ca2+, ATP facilitated the induction of afterdepolarizations and triggered activity in approximately 60% of the cells. In the presence of isoproterenol, ATP increased the amplitude of Iti and DADs by 55 and 206%, respectively, and caused increases in the amplitude of L-type Ca2+ current (ICa) and EADs, which occasionally led to triggered activity. Similarly, addition of ATP increased the amplitude of Iti and DADs induced by elevated extracellular Ca2+ by 110 and 83%, respectively. Ryanodine inhibited the ATP-induced increase in Iti but not the increase in ICa. In the presence of BAY K 8644 or quinidine, ATP not only further prolonged the action potential durations by 18 +/- 4 and 17 +/- 4%, respectively, but also increased the amplitude of EADs. The present results show a novel arrhythmogenic effect of extracellular ATP, which facilitates the genesis of triggered arrhythmias when Ca2+ influx is increased, probably by further increasing Ca2+ influx from extracellular medium and Ca2+ release from intracellular stores.

scholarly journals Existence of both fast and slow channel activity during the early stages of ventricular fibrillation.

1992 ◽  
Vol 70 (4) ◽  
pp. 773-786 ◽  
Author(s):  
X Zhou ◽  
P Guse ◽  
P D Wolf ◽  
D L Rollins ◽  
W M Smith ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Channel Activity ◽  
Early Stages ◽  
Slow Channel

scholarly journals Adaptations of vertebrate neurons to hypoxia and anoxia: maintaining critical Ca2+ concentrations.

1998 ◽  
Vol 201 (8) ◽  
pp. 1141-1152 ◽  
Author(s):  
P E Bickler ◽  
L T Buck
Keyword(s):  
Ion Channel ◽  
Action Potentials ◽  
G Protein Coupled Receptors ◽  
Channel Activity ◽  
Down Regulation ◽  
Inhibitory Neurotransmitters ◽  
Channel Arrest ◽  
Postsynaptic Receptors ◽  
G Protein Coupled ◽  
The Brain

Down-regulation of ion channel activity ('channel arrest'), which aids in preserving critical ion gradients in concert with greatly diminished energy production, is one important strategy by which anoxia-tolerant neurons adapt to O2 shortage. Channel arrest results in the elimination of action potentials and neurotransmission and also decreases the need for ion transport, which normally requires a large energy expenditure. Important targets of this down-regulation may be channels in which activity would otherwise result in the toxic increases in intracellular [Ca2+] characteristic of anoxia-sensitive mammalian neurons. In turtles, Na+ channels and the Ca2+-permeable ion channel of the N-methyl-d-aspartate (NMDA)-type glutamate receptor undergo down-regulation during anoxia. Inactivation of NMDA receptors during hypoxia occurs by a variety of mechanisms, including alterations in the phosphorylation state of ion channel subunits, Ca2+-dependent second messenger activation, changes in Ca2+-dependent polymerization/depolymerization of actin to postsynaptic receptors and activation of other G-protein-coupled receptors. Release of inhibitory neurotransmitters (e.g. gamma-aminobutyrate) and neuromodulators (e.g. adenosine) into the brain extracellular fluids may play an important role in the down-regulation of these and other types of ion channels.

Evidence for persistent activation of cardiac slow channels in low-calcium solutions

1982 ◽  
Vol 242 (5) ◽  
pp. H827-H833
Author(s):  
J. Linden ◽  
G. Brooker
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Slow Phase ◽  
Tetraacetic Acid ◽  
Channel Activation ◽  
Low Calcium ◽  
Slow Channel ◽  
Kinetics Of ◽  
Long Action

Action potentials were recorded from frog ventricular strips superfused with calcium-free solutions. Very long action potentials (3-60 s) were induced by chelating residual calcium with 1-5 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA). The kinetics of changes in action potential duration suggest that calcium influences action potential duration at an intracellular site. In low-calcium solutions isoproterenol was found to lengthen action potentials. The lengthening effect of isoproterenol became progressively greater as [Ca2+] was reduced by elevating [EGTA]. In the presence of 2 mM EGTA, 0.1 microM isoproterenol increased action potential duration from 4.3 +/- 0.4 to 43 +/- 14 s. Verapamil produced a greater than 90% reduction in the duration of very long action potentials (60 s) induced by EGTA, isoproterenol, or both. After rapid or prolonged depolarizations in low-calcium solutions the last 10-30 mV of repolarization took 10-15 s. We speculate that this slow phase of repolarization may be a manifestation of persistent slow channel activation. The data suggest that in low-calcium solutions slow channels can remain activated for many seconds.

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