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PubMed1991

Transient outward currents and action potential alterations in rabbit ventricular myocytes.

To clarify ionic mechanisms underlying successive changes in action potential repolarization upon sudden increase in driving rate or initiation of rapid drive after a rest, membrane potentials and currents were recorded from isolated rabbit ventricular myocytes using the suction-pipette whole-cell clamp method. When 20 action potentials were elicited with a stimulus frequency of 2.0 Hz after a rest period of 20 s, the plateau and action potential duration showed complex changes in successive beats, whereas they were nearly constant with stimulation at 0.1 Hz. There were only weak correlations between changes in action potential parameters and preceding diastolic intervals. The changes were prominent in the first 10 beats but subsided gradually thereafter, attaining nearly steady configurations of action potentials. When depolarizing pulses were applied at a fast rate, under the voltage clamp, the amplitudes of the initial inward current in the presence of tetrodotoxin changed greatly depending on the pulse numbers and diastolic intervals, whereas the delayed outward K+ current changed little. Variations of the initial inward current in successive pulses were caused by different degrees of activation and recovery from inactivation in the Ca2+ current, the Ca(2+)-sensitive and -insensitive transient outward current. While inhibition of either one or two current components decreased the action potential alterations, blocking the three components completely abolished them. These results indicate that alterations of the Ca(2+)-sensitive and -insensitive transient outward current together with the Ca2+ current contribute to the action potential alterations after initiation of rapid drive or an increase in driving rates.

Action Potentials↗

PubMed1977

On the relationship between action potential duration and tension in cat papillary muscle.

Tension and action potentials have been measured simultaneously from isolated cat papillary muscles. Two groups of experiments are described. In the first group, the external conditions under which the muscle contracted were changed. Specifically, stimulation rate, extra-cellular [Ca++], extracellular [Na++] were altered, and adrenaline was added to the bathing fluid. A tendency for given levels of tension to be accompanied by action potentials of constant duration is demonstrated under some of these conditions. In the second group of experiments, tension and action potentials were recorded following some change in external conditions; specifically, after a long rest, after a change in muscle length, and after the muscle had been set up in the experimental apparatus (the 'running-in' period). In the period that followed each of these interventions, peak tension increased substantially over at least several minutes but all external conditions (for example, temperature, muscle length, stimulation rate, and composition of the bathing fluid) remained constant. In each of these three situations tension increased but in one case the action potential duration increased, in another it decreased, and in the third it was unchanged. It is concluded that change in action potential durations do not necessarily make an important contribution to the changes in tension of papillary muscles.

Action Potentials↗

PubMed1977

Effects of adrenaline on the action potential of sympathetic ganglion cells in bullfrogs.

The effects of catecholamines (adrenaline, noradrenaline and isoproterenol) on ionic conductance changes during the generation of action potentials of bullfrog sympathetic and spinal ganglion cells were studied with intracellular microelectrodes. In sympathetic ganglion cells, adrenaline (3X10(-5)-1X10(-3)M) reversibly decreased the peak amplitude and positive after-potential of action potentials, and prolonged the duration of spike potentials without changes in the resting membrane potential and conductance in the Ringer solution. The maximum rates of rise and fall of spike potentials were also decreased. The action of noradrenaline was similar to that of adrenaline, but isoproterenol did not show any effects. Adrenaline (3X10(-5)-3X10(-4)M) markedly depressed the peak amplitude and maximum rate of rise of both TEA-potential and Ca-potential produced either in TEA solution containing TTX or in the isotonic CaCl2 solution. Similar actions were observed with noradrenaline but not isoproterenol. In spinal ganglion cells, catecholamines did not show any effects of the action potentials in Ringer and TEA solutions. It was concluded that adrenaline inhibited the increases in Ca2+, K+ and Na+ conductances during the generation of action potentials of sympathetic ganglion cells.

Action Potentials↗

PubMed1991

Control of action potentials and Ca2+ influx by the Ca(2+)-dependent chloride current in mouse pituitary cells.

1. Perforated patch recording was used to examine the influence of the calcium-dependent chloride current (iCl(Ca)) on Ca2+ action potentials in AtT-20 pituitary cells. The calculated chloride equilibrium potential (ECl) was adjusted by changing either intracellular or extracellular [Cl-]. Action potential duration varied as a function of ECl. When ECl was set at -21 mV, both spontaneous and evoked action potentials displayed a long plateau phase between -20 and -25 mV, which typically lasted for several seconds. Setting ECl to more negative potentials resulted in briefer action potentials; at an ECl of -52 mV, no plateau phase was evident. Spontaneous depolarization and action potential firing still occurred when ECl was negative to firing threshold, which indicates that the slow depolarizing wave that precedes the firing of spontaneous action potentials does not require activation of ICl(Ca). 2. In voltage clamp experiments the magnitude of ICl(Ca) diminished slowly during a prolonged depolarization, over a time course that coincided with action potential termination. 3. Niflumic acid (100 microM) blocked ICl(Ca) by 90% but had no effect on either K+ or Ca2+ currents. This concentration of niflumic acid eliminated the plateau phase, but did not prevent the firing, of Ca2+ action potentials. 4. Internal [Ca2+] was measured photometrically after loading cells with the Ca2+ indicator dye, Fura-2. Under voltage clamp conditions, concentrations of niflumic acid (30-100 microM) that blocked depolarization-evoked ICl(Ca) had little or no effect on simultaneously recorded Ca2+ transients. Perforated patch recording from Fura-loaded cells showed that action potentials were temporally associated with transient increases in intracellular [Ca2+]. Niflumic acid (30-100 microM) disrupted the rhythmic firing of spontaneous action potentials and associated intracellular Ca2+ transients. 5. Fluorescent measurements of Ca2+ transients were also made in cells unperturbed by patch recording, and were used as a measure of action potential duration in the absence of experimental alteration of internal [Cl-]. Spontaneous Ca2+ transients were of long duration (approximately 2 s), which suggests that intracellular [Cl-] is relatively high (40-50 mM) in these cells. The spontaneous Ca2+ transients were inhibited by niflumic acid. 6. Niflumic acid up to 100 microM, had neglible effects on either basal or stimulated (by 2 microM-(+/-)-isoprenaline) hormone secretion, as shown by radioimmunoassay of adrenocortotrophic hormone release.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2006

Unique features of action potential initiation in cortical neurons.

Neurons process and encode information by generating sequences of action potentials. For all spiking neurons, the encoding of single-neuron computations into sequences of spikes is biophysically determined by the cell's action-potential-generating mechanism. It has recently been discovered that apparently minor modifications of this mechanism can qualitatively change the nature of neuronal encoding. Here we quantitatively analyse the dynamics of action potential initiation in cortical neurons in vivo, in vitro and in computational models. Unexpectedly, key features of the initiation dynamics of cortical neuron action potentials--their rapid initiation and variable onset potential--are outside the range of behaviours described by the classical Hodgkin-Huxley theory. We propose a new model based on the cooperative activation of sodium channels that reproduces the observed dynamics of action potential initiation. This new model predicts that Hodgkin-Huxley-type dynamics of action potential initiation can be induced by artificially decreasing the effective density of sodium channels. In vitro experiments confirm this prediction, supporting the hypothesis that cooperative sodium channel activation underlies the dynamics of action potential initiation in cortical neurons.

Action Potentials↗

PubMed1998

The role of action potential prolongation and altered intracellular calcium handling in the pathogenesis of heart failure.

Action potential prolongation is a common finding in human heart failure and in animal models of cardiac hypertrophy. The mechanism of action potential prolongation involves altered expression of a variety of depolarising and hyperpolarising currents in the myocardium. In particular, decreased density of the transient outward potassium current seems to play a prominent role, regardless of species, precipitating factors or the severity of hypertrophy. The decreased density of the transient outward current appears to be caused by reduced transcription of Kv4.2 and Kv4.3 and may be caused in part by an inhibitory effect of alpha-adrenoceptor stimulation. During the early stage of the disease process, action potential prolongation may increase the amplitude of the intracellular calcium transient, causing positive inotropy. We argue therefore, that action prolongation may be a compensatory response which may acutely support the compromised cardiac output. In severe hypertrophy and end-stage heart failure however, despite continued action potential prolongation, the amplitude of the calcium transient becomes severely reduced. The mechanism underlying this event appears to involve reduced expression of calcium handling proteins, and these late events may herald the onset of failure. At present the events leading to the late changes in calcium handling are poorly understood. However, chronic activation of compensatory mechanisms including action potential prolongation may trigger these late events. In the present article we outline a hypothesis which describes a potential role for action potential prolongation, and the associated elevation in the levels of intracellular calcium, in maladaptive gene expression and the progression toward cardiac failure.

Action Potentials↗

PubMed1983

Action potential of isolated human ureter recorded with sucrose gap technique.

The action potential of human ureter was recorded in vitro by sucrose gap technique and the effects of some cations and drugs were studied. The action potential was composed of an initial fast component of spike and a subsequent slow component, a plateau, without a definite after-positive potential. Duration of the action potential was 1.0 +/- 0.1 (mean +/- standard deviation, n = 5) seconds at resting membrane potential level and 0.8 +/- 0.1 seconds at 90 per cent of the repolarization level. Ratio of plateau potential to spike potential was 80 +/- 4 per cent. The results of ionic influence suggested that calcium played an important role in the generation of spike potential and sodium in the generation of plateau potential. The application of noradrenaline and serotonin showed an excitatory effect which was observed as an increase of spontaneous discharge with depolarization of membrane potential and slow depolarization preceding the action potential. The slow depolarization was never observed in control preparations. These findings suggested that the ureter might have the capacity to generate a pacemaker-like slow depolarization which could conceivably relate to the automaticity of the ureter. Acetylcholine showed an excitatory effect only when the preparation was pretreated by physostigmine.

Action Potentials↗

PubMed1978

On the effects of divalent cations and ethylene glycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetate on action potential duration in frog heart.

Resting and action potentials were recorded from superfused strips of frog ventricle. Reducing the bathing calcium concentration ([Ca2+]0) with or without ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetate (EGTA) prolongs the action potential (AP). The change in the duration of the AP extends over many minutes, but is rapidly reversed by restoring calcium ions. Other changes (e.g., in resting potential and overshoot) are, however, only more slowly reversed. Reducing [Ca2+]0 with 0.2, 2, or 5 mM EGTA produces progressively greater prolongation of AP; maximum values were well in excess of 1 min. This prolongation can be reversed by other divalent cations in EGTA (Mg2+, Sr2+) or Ca-free (Mn2+) solutions, or by acetylcholine. Barium ions increase AP duration in keeping with their known effect on potassium conductance. D600, which blocks the slow inward current in cardiac muscle, is without effect on the action potentials recorded in EGTA solutions, or on the time course and extent of the recovery to normal duration upon restoring calcium ions. It is concluded that divalent cations exert an influence on membrane potassium conductance extracellularly in frog heart. The cell membrane does not become excessively "leaky" in EGTA solutions.

Acetylcholine↗

PubMed1987

Effects of activation sequence and anisotropic cellular geometry on the repolarization phase of action potential of dog ventricular muscles.

The influence of activation sequences on action potential configuration, especially in the repolarization phase, was examined in isolated canine ventricular muscles. Action potentials were recorded from the epicardial surface in the center of a preparation having nearly uniform fiber orientation (25 X 25 mm). Stimuli applied just adjacent to the recording site produced nearly centrifugal propagation. An activation sequence either parallel (longitudinal) or perpendicular (transverse) to the long axis of the muscle fibers was produced by peripheral stimulation. Action potential duration at -60 mV (APD-60 mV) during centrifugal propagation was significantly longer than that during longitudinal propagation. Further shortening of APD-60 mV was observed during transverse propagation. When a collision of longitudinal or transverse wavefronts (longitudinal or transverse collision) was produced at the action potential recording site, the shortest APD was recorded. During centrifugal propagation, action potential mapping around the stimulating electrodes revealed that APD-60 mV shortened gradually as the recording site was moved further from the stimulation site. The spatial gradient of APD was steeper in the transverse than in the longitudinal direction, causing a distortion in the repolarization sequence and the recovery of excitability near the center of the tissue. Premature stimuli applied to an area near the central stimulation site induced one-way block and circus movement of the wavefront, indicating reentry of excitation. We concluded that the activation sequence and anisotropic cellular geometry substantially affect APD, and that such a change contributes to the spatial inhomogeneity of refractoriness leading to reentrant arrhythmias.

Action Potentials↗

PubMed1988

Hypothermic effects on action potential and force production of hedgehog and guinea pig papillary muscles.

Action potentials and isometric force were recorded in papillary muscles from guinea pigs and summer hedgehogs at different temperatures between 37 and 0 degrees C. The action potential of the hedgehog was of a lower amplitude (mean 83 +/- 6 mV) than that of the guinea pig (mean 110 +/- 5 mV). The action potential duration at 50% repolarization was 22 +/- 2 msec in the hedgehog as compared to 105 +/- 11 msec in the guinea pig. Moreover, there was no distinct plateau phase of the hedgehog action potential. Lowering temperature prolonged the action potential duration in the two preparations by about the same percentage. However, the guinea pig preparation became progressively less excitable below 20 degrees C. Lowered temperature produced a positive inotropic effect in the guinea pig, whereas this effect was very slight in the hedgehog heart. Postextrasystolic potentiation was seen in the guinea pig but not in the hedgehog preparation. It is suggested that this difference between the preparations may be due to a greater relative amount of activator calcium in the hedgehog heart. The difference in cold tolerance between the preparations may reflect a difference in chemical composition of the sarcolemma.

Action Potentials↗

PubMed1994

Monophasic action potentials: concepts to practical applications.

Monophasic action potential (MAP) recordings reproduce the repolarization time course of intracellular action potentials with high accuracy and provide precise information on the local activation time. With the advantage of in vivo application and the development of the safer and simpler contact catheter technique, MAP recording has become the method of choice for evaluating myocardial repolarization changes. This review aims to provide information on practical application of MAP recording in the clinical setting. MAPs can easily be recorded from the endocardium with the contact catheter technique in the electrophysiology laboratory and from the epicardium with electrode probes during open heart surgery. The technical aspects are described in detail. The rate dependence of myocardial excitability and repolarization and the effect of antiarrhythmic drugs on MAP duration and effective refractory period are thoroughly reviewed. The use of MAPs in detecting myocardial ischemia, in studying early afterdepolarization and triggered arrhythmias, in measuring dispersion of repolarization, in identifying intracardiac conduction and the development of the T wave, and in verifying the arrhythmogenic effect of mechanoelectric feedback are presented. Computerized automatic analysis of MAPs and the limitations of the MAP technique are also discussed.

Action Potentials↗

PubMed2003

Modulation of action potential firing by iberiotoxin and NS1619 in rat dorsal root ganglion neurons.

The present study investigated the effects of iberiotoxin (IbTx), a peptide toxin blocker of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels and NS1619, a BK(Ca) channel opener, on action potential firing of small and medium size afferent neurons from L6 and S1 dorsal root ganglia of adult rats. Application of IbTx (100 nM) reduced whole-cell outward currents in 67% of small and medium size neurons. Analysis of action potential profile revealed that IbTx significantly prolonged the duration of action potential and increased firing frequency of afferent neurons. IbTx did not significantly alter the resting membrane potential, threshold for action potential activation and action potential amplitude. The benzimidazolone NS1619 (10 microM) increased opening activity of a Ca(2+)-dependent channel as assessed by single channel measurements. In contrast to IbTx, NS1619 reversibly suppressed action potential firing, attributable to increases in threshold for evoking action potential, reduction in action potential amplitude and increases in amplitude of afterhyperpolarization. The effect of NS1619 on neuronal firing was sensitive to IbTx, indicating the attenuation of neuronal firing by NS1619 was mediated by opening BK(Ca) channels. NS1619 also reduced neuronal hyperexcitability evoked by 4-aminopyridine (4-AP), a transient-inactivated K(+) channel (A-current) blocker, in an IbTx-sensitive manner. These results indicate that IbTx-sensitive BK(Ca) channels exist in both small and medium diameter dorsal root ganglion (DRG) neurons and play important roles in the repolarization of action potential and firing frequency. NS1619 modulates action potential firing and suppresses 4-AP-evoked hyperexcitability in DRG neurons, in part, by opening BK(Ca) channels. These results suggest that opening BK(Ca) channels might be sufficient to suppress hyperexcitability of afferent neurons as those evoked by stimulants or by disease states.

Action Potentials↗

PubMed1995

[Simulation of myocardial action potentials of various cell types in relation to neural parameters].

Action potentials of various myocardial cell types were simulated in a computer model based on current knowledge of the electrical properties of ionic channels and pumps in the ventricular cell membrane and the sarcoplasmic reticulum. The transport mechanisms of sodium, potassium, calcium and chlorine ions through the cell membrane are described mathematically, as is the exchange of calcium between the myoplasm and sarcoplasmic reticulum. Ten ionic channels and three pumps of the cell membrane are taken into account, while three channels and one pump of the sarcoplasmic reticulum are considered in the computations. For the first time, the transient outward potassium current IK,to was simulated, the effect of which on the early repolarisation phase of the action potential was reproducible in the model. Calcium buffers in the myoplasm and the sarcoplasmic reticulum are also considered. From the resulting ionic currents through the channels and pumps, the membrane potential is computed using an equivalent circuit diagram of the cell membrane. In particular the influence of neural activity on channel conductance and the probability of channel patency were taken into account. By means of this model, different shapes of ventricular action potentials were simulated. The action potentials of epicardial cells, M-cells, endocardial cells and Purkinje fibres were accurately simulated. In addition, the effects of sympathetic drive and various drugs were demonstrated in the model as well as the shortening of the action potential duration with increasing stimulation frequency.

Calcium↗

PubMed1985

The different intracellular action potentials of fast and slow muscle fibres.

The time course of the intracellular action potential was studied quantitatively, because it is an important factor in the generation of electromyographic signals. In in vivo preparations of the m. EDL and m. soleus of the rat single motor units were stimulated and intracellular action potentials were recorded in muscle fibres belonging to those motor units. In this arrangement it was possible to relate the intracellular action potential to the fibre type. The intracellular action potentials of fast twitch glycolytic (FTG) EDL and of slow soleus fibres were described, using 8 characteristics. All characteristics but one differed significantly between the two fibre populations. Comparing characteristics of intracellular action potentials of FTG fibres with slow fibres, it is concluded that: the resting membrane potential is more negative; the amplitude of the action potential is larger; the maximum rates of depolarization and repolarization are higher; and the shape of the repolarization phase is more variable.

Action Potentials↗

PubMed2000

Differential effects of K(+) channel blockers on frequency-dependent action potential broadening in supraoptic neurons.

Recordings were made from magnocellular neuroendocrine cells dissociated from the supraoptic nucleus of the adult guinea pig to determine the role of voltage gated K(+) channels in controlling the duration of action potentials and in mediating frequency-dependent action potential broadening exhibited by these neurons. The K(+) channel blockers charybdotoxin (ChTx), tetraethylammonium (TEA), and 4-aminopyridine (4-AP) increased the duration of individual action potentials indicating that multiple types of K(+) channel are important in controlling action potential duration. The effect of these K(+) channel blockers was almost completely reversed by simultaneous blockade of voltage gated Ca(2+) channels with Cd(2+). Frequency-dependent action potential broadening was exhibited by these neurons during trains of action potentials elicited by membrane depolarizing current pulses presented at 10 Hz but not at 1 Hz. 4-AP but not ChTx or TEA inhibited frequency-dependent action potential broadening indicating that frequency-dependent action potential broadening is dependent on increasing steady-state inactivation of A-type K(+) channels (which are blocked by 4-AP). A model of differential contributions of voltage gated K(+) channels and voltage gated Ca(2+) channels to frequency-dependent action potential broadening, in which an increase of Ca(2+) current during each successive action potential is permitted as a result of the increasing steady-state inactivation of A-type K(+) channels, is presented.

4-Aminopyridine↗

PubMed1977

Modulation of cyclic nucleotide levels in peripheral nerve without effect on resting or compound action potentials.

1. Cyclic nucleotide levels and compound action potential magnitudes were measured in frog sciatic nerves following exposure to carbachol, isoprenaline and cyclic nucleotide related substances. 2. The resting cyclic AMP level was 2-4 p-mole/mg protein and the cyclic GMP level was 0-27 p-mole/mg protein in desheathed nerves. 3. Isoprenaline (100 micrometer) caused a twofold increase in cyclic AMP without affecting cyclic GMP levels. Carbachol (100 micrometer) caused a twofold increase in cyclic GMP without affecting cyclic AMP levels. 4. The phosphodiesterase inhibitor theophylline (5 mM) augmented both cyclic AMP and cyclic GMP. 5. The magnitude of the resting or compound action potential was not affected by isoprenaline, carbachol, or phosphodiesterase inhibitors. 6. The cyclic nucleotides and their butyryl derivatives did not affect the magnitude of the resting or compound action potential, either when applied alone or in the presence of a phosphodiesterase inhibitor. 7. In contrast to sympatic tissue we conclude that hormone mediated cyclic nucleotide metabolism in peripheral nerve is unrelated to control of axonal excitability.

Action Potentials↗

PubMed1993

Effects of 3,6-dimethylamino-dibenzopyriodonium edetate on action potentials in guinea pig papillary muscles.

The effects of 3,6-dimethylamino-dibenzopyriodonium edetate (IHC-72) on action potentials (AP) and slow response action potentials of guinea pig papillary muscles were studied with intracellular microelectrodes. IHC-72 12.7, 25.4, and 50.8 mumol.L-1 decreased the maximal upstroke velocity (Vmax), amplitude of action potential (APA), over shot (OS), and resting potential (RP) while prolonged the action potential duration at 30%, 50%, 90%, and 100% repolarization (APD30, APD50, APD90, and APD100). IHC-72 25.4 and 50.8 mumol.L-1 decreased the APA, Vmax, and prolonged APD50 and APD90 under high K+ superfusion. IHC-72 25.4 and 50.8 mumol.L-1 depressed the automaticity, APA, and maximal diastolic potential (MDP) of the slow response action potentials induced by BaCl2. The results indicated that IHC-72 might nonspecifically inhibit the transmembrane movement of Ca2+, Na+, and K+.

Action Potentials↗

PubMed1993

Developmental changes in action potential properties of the guinea-pig myocardium.

Developmental changes in action potential properties were examined in electrically driven (1 Hz) left atria and right ventricles from foetal, neonatal and adult guinea-pig hearts, using standard micro-electrode recording techniques. In both left atria and right ventricles, the overshoot, resting potential and maximum upstroke velocity of the action potential increased progressively with age until birth, and then remained almost unchanged. Action potential duration (APD) changed markedly with age during foetal and neonatal periods. In left atria, APD at 50% repolarization initially decreased until foetal day 50, and then increased until the adult period. In right ventricles, APD initially increased until approximately foetal day 45, then decreased for 5 days following birth, thereafter it increased again. In addition, after-hyperpolarization was observed only in left atria of younger foetuses. Thus we have demonstrated that in the guinea-pig myocardium developmental changes in action potential properties occur more extensively during the foetal period than during the postnatal period.

Action Potentials↗