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PubMedDate not supplied

The monophasic action potential: a simple in vivo model to evaluate the effects of antiarrhythmic drugs at atrial level.

Monophasic action potential (MAP) represents an extracellular recording of electrical potentials variations produced simultaneously by several cells. Even if it does not represent the real cellular action potential, monophasic action potential generally reproduces with accuracy that aspect, being useful especially in the assessment of myocardial repolarisation phases. Monophasic action potential recording was performed with a quadripolar catheter designed by Franz; the quality of recordings was good and the procedure is safe. In clinical electrophysiology, monophasic action potential may be helpful in the study of certain aspects that cannot be evaluated adequately by standard electrophysiological techniques. The study was performed on six patients, in drug-free state. The duration of monophasic action potential at 90% of repolarisation and the atrial effective refractory period, at three basic cycle lengths (600, 500 and 400 msec) were determined. Both monophasic action potential duration at 90% of repolarisation and the atrial effective refractory period shortening at short cycle length and a linear correlation between these two parameters were seen. We conclude that the correlation between monophasic action potential duration and the effective atrial refractory period may be a simple and useful model to characterise in vivo the electrophysiologic profile of antiarrhythmic drugs.

Action Potentials↗

PubMed2000

Microcomputer program for automated action potential waveform analysis.

A program for action potential waveform analysis based on a PC compatible computer is described. Single or averaged action potentials are analyzed by obtaining its first derivative and using criteria which allow automatic measurement of several action potential components, including: depolarization rate, repolarization rate, amplitude, duration, resting membrane potential and afterhyperpolarization amplitude and slope. Data can be imported from pClamp (Axon Instruments) and exported to other software such as Excel, Sigmaplot and MatLab for example.

Action Potentials↗

PubMed1995

Magnetic-evoked compound muscle action potential neuromonitoring in spine surgery.

STUDY DESIGN: Muscle action potentials elicited by paired transcranial magnetic stimulation were recorded during spine surgery in 34 patients. Anesthesia was based on ketamine and fentanyl. OBJECTIVES: To evaluate the optimal anesthetic regimen to be used for transcranial magnetic stimulation, and to determine the clinical import of magnetic-evoked compound muscle action potentials. SUMMARY OF BACKGROUND DATA: Muscle action potential by transcranial magnetic stimulation has been difficult to record under general anesthesia. Ketamine is known to not suppress the muscle responses, although no conclusive clinical study has been reported. METHODS: Paired transcranial magnetic stimulation was delivered as muscle action potentials were recorded from the limb musculature. RESULTS: Neuromonitoring was reliable in 56% of total cases and in 82% of the recent cases after reducing fentanyl dosage. Paired magnetic stimulation was an excellent facilitation technique for reliable monitoring. At higher dosages, fentanyl and ketamine decreased the reproducibility of the responses. CONCLUSIONS: Magnetic-evoked compound muscle action potential neuromonitoring is a sensitive and selective motor pathway monitoring method that covers the entire motor pathway, including the white and gray matter of the spinal cord. Ketamine-based anesthesia is a good choice for this purpose.

Action Potentials↗

PubMed1987

Differential effects of isoproterenol on the canine atrial action potential in the presence of carbachol or nicorandil.

In canine atrial muscles, carbachol and nicorandil hyperpolarized the resting membrane potential and shortened the action potential duration. In the presence of carbachol or nicorandil, isoproterenol further hyperpolarized the resting membrane potential and shortened the action potential duration. Isoproterenol significantly increased the plateau duration in the presence of nicorandil, but further abbreviated it in the presence of carbachol. This increase in the plateau duration by isoproterenol in the presence of nicorandil probably reflects the increase in the slow inward current.

Action Potentials↗

PubMed2005

Model-based source localization of extracellular action potentials.

A new model-based analysis method was set up for revealing information encrypted in extracellular spatial potential patterns of neocortical action potentials. Spikes were measured by extracellular linear multiple microelectrode in vivo cat's primary auditory cortex and were analyzed based on current source density (CSD) distribution models. Validity of the monopole and other point source approximations were tested on the measured potential patterns by numerical fitting. We have found, that point source models could not provide accurate description of the measured patterns. We introduced a new model of the CSD distribution on a spiking cell, called counter-current model (CCM). This new model was shown to provide better description of the spatial current distribution of the cell during the initial negative deflection of the extracellular action potential, from the onset of the spike to the negative peak. The new model was tested on simulated extracellular potentials. We proved numerically, that all the parameters of the model could be determined accurately based on measurements. Thus, fitting of the CCM allowed extraction of these parameters from the measurements. Due to model fitting, CSD could be calculated with much higher accuracy as done with the traditional method because distance dependence of the spatial potential patterns was explicitly taken into consideration in our method. Average CSD distribution of the neocortical action potentials was calculated and spatial decay constant of the dendritic trees was determined by applying our new method.

Action Potentials↗

PubMed1990

Chloride action potentials and currents in embryonic skeletal muscle of the chick.

Chloride-dependent action potentials were elicited from embryonic skeletal muscle fibers of the chick during the last week of in ovo development. The duration of the action potentials was extremely long (greater than 8 sec). The action potentials were reversibly blocked by the stilbene derivative, SITS, a specific blocker of chloride permeability. Using patch clamp pipettes, in which the intracellular chloride concentration was controlled and with other types of ion channels blocked, the membrane potential at the peak of the action potential closely coincided with the chloride equilibrium potential calculated from the Nernst equation. These data indicate that activation of a chloride-selective conductance underlies the long duration action potential. The occurrence of the chloride-dependent action potential was found to increase during embryonic development. The percentage of fibers that displayed the action potential increased from approximately 20% at embryonic day 13 to approximately 70% at hatching. Chloride-dependent action potentials were not found in adult fibers. The voltage and time-dependent currents underlying the action potential were recorded under voltage clamp using the whole-cell version of the patch pipette technique. The reversal potential of the currents was found to shift with the chloride concentration gradient in a manner predicted by the Nernst equation, and the currents were blocked by SITS. These data indicate that chloride ions were the charge carriers. The conductance was activated by depolarization and exhibited very slow activation and deactivation kinetics.

Action Potentials↗

PubMed1991

[Effects of metoclopramide on slow response action potentials of myocardium].

The effects of metoclopramide (Met) on the action potential of rabbit sinus node cells and slow response action potential of guinea pig papillary muscles were studied with the intracellular microelectrodes. Met 10 mumol.L-1 prolonged the action potential duration at 90% repolarization (APD90) of SA node cell and sinus cycle length (SCL). Met 100 mumol.L-1 caused a decrease in action potential amplitude (APA), Vmax and the slope of phase 4 of action potential of SA node cell. APD90 and SCL were prolonged further. For slow response action potential induced by KCl (25 mmol.L-1), Met 100 mumol.L-1 produced a decrease in APA and depolarization rate. Met 10 mumol.L-1 began to suppress the spontaneous electrical activities induced by barium ion. These findings suggest that Met probably has the effect of blocking calcium inward current in myocardium.

Action Potentials↗

PubMed2002

Action potential afterdepolarization mediated by a Ca2+-activated cation conductance in myenteric AH neurons.

We investigated the nature of afterdepolarizing potentials in AH neurons from the guinea-pig duodenum using whole-cell patch-clamp recordings in intact myenteric ganglia. Afterdepolarizing potentials were minimally activated following action-potential firing under normal conditions, but after application of charybdotoxin (40 nM) or tetraethyl ammonium (TEA; 10-20 mM) to the bathing solution, prominent afterdepolarizing potentials followed action potentials. The whole-cell current underlying afterdepolarizing potentials (I(ADP)) in the presence of TEA (10-20 mM) reversed at -38 mV and was not voltage-dependent. Reduction of NaCl in the bathing (Krebs) solution to 58 mM shifted the reversal potential of the I(ADP) to -58 mV, suggesting that the current underlying the afterdepolarizing potential was carried by a mixture of cations. The relative contributions of Na(+) and K(+) to this current were estimated to be about 1:5. Substitution of external Na(+) with N-methyl D-glucamine blocked the current while replacement of internal Cl(-) with gluconate did not block the I(ADP). The I(ADP) was also inhibited when CsCl-filled patch pipettes were used. The I(ADP) was blocked or substantially decreased in amplitude in the presence of N-type Ca(2+) channel antagonists, omega-conotoxin GVIA and omega-conotoxin MVIIC, respectively, and was eliminated by external Cd(2+), indicating that it was dependent on Ca(2+) entry. The I(ADP) was also inhibited by ryanodine (10-20 microM), indicating that Ca(2+)-induced Ca(2+) release was involved in its activation. Niflumic acid consistently inhibited the I(ADP) with an IC(50) of 63 microM. Using antibodies against the pore-forming subunits of L-, N- and P/Q-type voltage-gated Ca(2+) channels, we have demonstrated that myenteric AH neurons express N- and P/Q, but not L-type voltage-gated Ca(2+) channels. We conclude that the ADP in myenteric AH neurons, in the presence of an L-type Ca(2+)-channel blocker, is generated by the opening of Ca(2+)-activated non-selective cation channels following action potential-mediated Ca(2+) entry mainly through N-type Ca(2+) channels. Ca(2+) release from ryanodine-sensitive stores triggered by Ca(2+) entry contributes significantly to the activation of this current.

Action Potentials↗

PubMed1983

Rabbit atrial myocardium in hypoxic conditions: rate dependent variation of action potential.

The dependence of the repolarization phase of the action potential in the atrial myocardium on the pacing pattern was studied in normoxic and hypoxic conditions. Intracellular action potentials were recorded by means of the conventional microelectrode technique from isolated left atrial trabeculae of the rabbit. By varying the pacing pattern and the oxygen supply changes of the configuration of action potential and of the membrane current as well as a conductance measure gK were obtained. In all pacing patterns the duration of action potentials is shortened, and the net outward current is enhanced by hypoxia. In steady state and for premature action potentials, gK is enlarged by hypoxia, but in action potentials after a pacing pause it is diminished more in hypoxic than in normoxic conditions. The findings suggest inhibition of an inward current in hypoxia as well as a dependence of a potassium background conductance on the inner Ca-concentration in normoxic and hypoxic conditions.

Action Potentials↗

PubMed1991

The cytosolic calcium transient modulates the action potential of rat ventricular myocytes.

1. The modulation of the action potential by the cytosolic Ca2+ (Cai2+) transient was studied in single isolated rat ventricular myocytes loaded with the acetoxymethyl ester form of the Ca(2+)-sensitive fluorescent dye Indo-1. Stimulation following rest and exposure to ryanodine were used to change the amount of Ca2+ released from the sarcoplasmic reticulum and thus the size of the Cai2+ transient. The Cai2+ transient was measured as the change, upon stimulation, in the ratio of Indo-1 fluorescence at 410 nm to that at 490 nm (410/490) and action potentials or membrane currents were recorded using patch-type microelectrodes. 2. When stimulation was initiated following rest, the magnitude of the Cai2+ transient decreased in a beat-dependent manner until a steady state was reached. The negative staircase in the Cai2+ transient was accompanied by a similar beat-dependent decrease in the duration of the action potential, manifested primarily as a gradual loss of the action potential plateau (approximately -45 mV). A slow terminal phase of repolarization of a few millivolts in amplitude was found to parallel the terminal decay of the Cai2+ transient. 3. The terminal portion of phase-plane loops of membrane potential (Vm) vs. Indo-1 ratio from all of the beats of a stimulus train followed a common linear trajectory even though the individual beats differed markedly in the duration and amplitude of the action potential and Cai2+ transient. 4. When the stimulation dependence of the Cai2+ transient was titrated away with submaximal exposure to ryanodine, the stimulation-dependent changes in the action potential plateau and terminal phase of repolarization were also eliminated. The same effect was noted in cells which, fortuitously, did not show a staircase in the Cai2+ transient following a period of rest. 5. When action potentials were triggered immediately following spontaneous release of Ca2+ from the sarcoplasmic reticulum, which results in a small depolarization at the resting potential, phase-plane loops (Vm vs. Indo-1 ratio) of the spontaneous events followed the same linear trajectory as the terminal phase of repolarization in the loops of the stimulated beats. 6. Following repolarization from brief voltage clamp pulses (to minimize time and voltage-dependent currents associated with depolarization), an inward current was observed that rose and fell in phase with the Cai2+ transient. This current was present at -70 mV, near the resting potential, and at -40 mV, a potential relevant to the plateau of the action potential.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1999

Motor unit action potential duration and muscle length.

Motor unit action potential (MUAP) components are investigated by means of single fiber computer simulations and clinical measurements. The single fiber simulations have essentially full bandwidth without noise, whereas the clinical measurements were made with a 3-10,000-Hz bandwidth utilizing approximately 1000 averages to reduce noise optimally. These parameters allow the recording of a MUAP's complete "physiologic" duration including its very slow onset and termination. The simulation results demonstrate a constant waveform onset regardless of the electrode's recording location along the fiber. A far-field potential is initiated when the action potential encounters the muscle fiber's termination. The simulated waveform's and clinically recorded MUAP's near-field component extends between the potential's onset and its corresponding far-field potential's onset. This near-field component's duration should vary with fiber length, and this prediction is clinically confirmed by measuring three different muscle lengths. The far-field potential reveals a constant duration, independent of fiber length, and appears to be associated with the muscle fiber's intracellular action potential duration. A more complete understanding of the components contributing to MUAP duration should provide a more fundamental basis for quantitative clinical MUAP duration measurements.

Action Potentials↗

PubMed1989

Characteristics of cardiac action potentials in marsupials.

Standard microelectrode techniques were used to record action potentials from single atrial, ventricular and Purkinje fibers of hearts taken from three species of marsupial (Macropus rufus, Macropus robustus and Macropus eugenii) and from dogs, sheep and guinea-pigs. The major electrophysiological parameters of marsupial potentials were qualitatively similar to the values for placental mammals. The grouped data for ventricular action potentials from studies on 6 adult male red kangaroos (Macropus rufus) were (mean +/- SD): Resting potential -69.5 +/- 5.0 mV; action potential amplitude 92.7 +/- 5.7 mV; action potential duration (to 90% repolarization): 182.5 +/- 17.5 ms; maximum rate of depolarization: 196.5 +/- 80.1 V/s. The major point of difference was the short duration of the red kangaroo ventricular action potential compared to those of the placental mammals, and compared to atrial cells from the kangaroos. It is suggested that this explains the short QT interval reported by others for kangaroo electrocardiograms, and that it may also be implicated in the high frequency of sudden death previously noted in these animals.

Action Potentials↗

PubMedDate not supplied

Effects of verapamil and lidocaine on changes in action potential characteristics and conduction time induced by combined hypoxia, hyperkalemia, and acidosis in canine ventricular myocardium.

We examined the effects of verapamil and lidocaine on changes in action potential characteristics and conduction time in the isolated right ventricular myocardium of canine hearts during superfusion with altered Tyrode's solution imitating some of metabolic alterations that occur in acute myocardial ischemia (Po2 less than 50 mm Hg, KCl 8 mM, pH 6.80). Altered Tyrode's solution produced loss of resting membrane potential (RMP), action potential amplitude (APA), action potential duration, and upstroke velocity of action potential (Vmax), and prolonged conduction time (CT). In the presence of lidocaine (5 mg/L), altered Tyrode's solution aggravated the reductions of APA and Vmax and the prolongation of CT in both endocardial and epicardial muscle cells. On the other hand, in the presence of verapamil (1 mg/L), the degree of the reductions of APA and Vmax and of the prolongation of CT induced by altered Tyrode's solution was reduced in epicardial muscle cells, but not in endocardial ones. Neither verapamil nor lidocaine affected change in RMP. These results suggest that the improving effect of verapamil on ischemia-induced conduction delay can be partly explained by its salutary effect on the depressed fast channel.

Acidosis↗

PubMed1984

Strontium, nifedipine and 4-aminopyridine modify the time course of the action potential in cells from rat ventricular muscle.

Action potentials, initiated by brief depolarizing pulses, were recorded from single cells isolated from rat ventricular muscle. These action potentials showed a rapid upstroke to about +30 mV, followed by two phases of repolarization referred to as the early and late phases of the action potential. Nifedipine (1 microM), which blocks the second inward current (Isi) carried by Ca in these cells, shortened the early phase. Substitution of strontium for calcium in the solution bathing the cells, a procedure which prolongs Isi, prolonged the early phase. 4-Aminopyridine (1 mM), which inhibits transient outward current, prolonged the early phase with either calcium or strontium in the external solution. It is concluded that both Isi and transient outward current contribute to the early phase of the action potential in rat ventricular muscle. It is also suggested that Isi does not directly contribute to the late phase, since the characteristics of the late phase are not compatible with such a role, and the possibility of additional inward current is investigated in the accompanying paper (Mitchell et al., 1984).

4-Aminopyridine↗

PubMed1985

Action potentials dependent on monovalent cations in developing mouse embryos.

Action potentials were examined using intracellular recording techniques to study the ionic mechanisms of excitability in oocytes and embryos of the mouse from the 1-cell through to the 16-cell stages of development. At all stages examined, action potentials dependent on monovalent cations (Na+ or Li+) were observed under Ca2+-free conditions, and the maximum rate of rise (MRR) of the Na action potential was larger than that of the Li action potential at a given concentration of monovalent cations. Both the Na and Li action potentials were insensitive to tetrodotoxin, and they were blocked by inorganic (Co2+, Cd2+, Mn2+, La3+) and organic (diltiazem) Ca antagonists. These properties were exactly the same as those of the Ca channels present in the membranes of the mouse embryos. In addition, competition was observed between permeant monovalent and divalent cations: the overshoot and MRR of the Na or Li action potentials were reduced in the presence of Ca2+. These results suggest that Na+ or Li+ go through the Ca channels when the external Ca2+ concentration was very low, and that the Ca channels are more permeable to Na+ than to Li+. Separate Na channels could not be detected or induced at any stages of development.

Action Potentials↗

PubMed1992

Evidence that action potentials activate an internodal potassium conductance in lizard myelinated axons.

1. We have studied action potentials and after-potentials evoked in the internodal region of visualized lizard intramuscular nerve fibres by stimulation of the proximal nerve trunk. Voltage recordings were obtained using microelectrodes inserted into the axon (intra-axonal) or into the layers of myelin (peri-internodal), with the goal of studying conditions required to activate internodal K+ currents. 2. Peri-internodal recordings made using K2SO4-, KCl- or NaCl-filled electrodes exhibited a negligible resting potential (less than 2 mV), but showed action potentials with peak amplitudes of up to 78 mV and a duration less than or equal to that of the intra-axonally recorded action potential. 3. Following ionophoretic application of potassium from a peri-internodal microelectrode, the peri-internodal action potential was followed by a prolonged (hundreds of milliseconds) negative plateau. This plateau was not seen following peri-internodal ionophoresis of sodium. The prolonged negative potential (PNP) was confined to the K(+)-injected internode: it could be recorded by a second peri-internodal microelectrode inserted into the same internode, but not into an adjacent internode. 4. The peri-internodally recorded PNP was accompanied by an equally prolonged intra-axonal depolarizing after-potential, and by an increase in the conductance of the internodal axolemma. However, the K+ ionophoresis that produced the PNP had little or no detectable effect on the intra-axonally or peri-internodally recorded resting potential or action potential. These findings suggest that the PNP is generated by an inward current across the axolemma of the K(+)-injected internode, through channels opened following the action potential. 5. Following peri-internodal K+ ionophoresis a PNP could also be evoked by passage of depolarizing current pulses through an intra-axonal electrode or by passage of negative current pulses through an electrode in the K(+)-filled peri-internodal region. The threshold for evoking a PNP was less than the threshold for evoking an action potential, and the PNP persisted in 10 microM-tetrodotoxin. Thus the PNP is evoked by depolarization of the axolemma rather than by Na+ influx. 6. The PNP was reversibly blocked by tetraethylammonium (TEA, 2-10 mM), but was not blocked by 100 microM-3,4-diaminopyridine or 5 mM-4-aminopyridine.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1998

Development of ionic currents underlying changes in action potential waveforms in rat spinal motoneurons.

Development of ionic currents underlying changes in action potential waveforms in rat spinal motoneurons. J. Neurophysiol. 80: 3047-3061, 1998. Differentiation of the ionic mechanism underlying changes in action potential properties was investigated in spinal motoneurons of embryonic and postnatal rats using whole cell voltage- and current-clamp recordings. Relatively slow-rising, prolonged, largely Na+-dependent action potentials were recorded in embryonic motoneurons, and afterdepolarizing potentials were elicited in response to prolonged intracellular injections of depolarizing currents. Action potential amplitude, as well as its rates of rise and repolarization significantly increased, and an afterhyperpolarizing potential (AHP) became apparent immediately after birth. Concurrently, repetitive action potential firing was elicited in response to a prolonged current injection. To determine the ionic mechanism underlying these changes, the properties of voltage-gated macroscopic Na+, Ca2+, and K+ currents were examined. Fast-rising Na+ currents (INa) and slow-rising Ca2+ currents (ICa) were expressed early in embryonic development, but only INa was necessary and sufficient to trigger an action potential. INa and ICa densities significantly increased while the time to peak INa and ICa decreased after birth. The postnatal increase in INa resulted in overshooting action potential with significantly faster rate of rise than that recorded before birth. Properties of three types of outward K+ currents were examined: transient type-A current (IA), noninactivating delayed rectifier-type current (IK), and Ca2+-dependent K+ current (IK(Ca)). The twofold postnatal increase in IK and IK(Ca) densities resulted in shorter duration action potential and the generation of AHP. Relatively large IA was expressed early in neuronal development, but unlike IK and IK(Ca) its density did not increase after birth. The three types of K+ channels had opposite modulatory actions on action potential firing behavior: IK and IA increased the firing rate, whereas IK(Ca) decreased it. Our findings demonstrated that the developmental changes in action potential waveforms and the onset of repetitive firing were correlated with large increases in the densities of existing voltage-gated ion channels rather than the expression of new channel types.

Action Potentials↗

PubMed1986

Differential effects of trichothecenes on the canine cardiac action potential.

We investigated the hypothesis that trichothecenes directly alter cardiac electrical activity. Action potentials were recorded from electrically stimulated canine false tendons before, during and after exposure to trichothecenes (1.0 mg/l). Action potentials recorded prior to and 60 min after exposure to trichothecenes were compared statistically. T-2 toxin decreased resting potentials in interventricular septum cells (7%), decreased action potential durations in papillary muscle cells (19%) and decreased both in false tendon cells (11% and 27%, respectively). Scirpentriol shortened durations of action potentials recorded in false tendon cells (24%), but had no other effects on any of the cell types tested. T-2 tetraol shortened the duration of interventricular septum cell action potentials (35%), but had no significant effects on other cardiac cells. Adenosine-5'-triphosphate (ATP) (final concentration 1100 mg/l) reversed all the effects of the trichothecenes on canine cardiac action potentials. These action potential changes may reflect a deficit of high energy phosphate and directly contribute to trichothecene-induced arrhythmias.

Action Potentials↗