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PubMed1979

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

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.

Action Potentials↗
PubMed1992

[The effect of anesthetic agents on descending spinal cord evoked potential and the compound muscle action potentials elicited by stimulation at the cerebral motor cortex and the spinal cord].

Recently, intraoperative monitoring of the motor tract by descending spinal cord motor evoked potentials (MEP) and compound muscle action potentials (CMAP) has been applied in clinical testing. Since several reports have mentioned the vulnerability of these potentials to anesthetic agents, experimental studies were carried out on the relationship between these potentials and anesthesia using 41 adult cats. The effects of anesthesia on changes in amplitude of the direct wave (D wave) and indirect wave (I wave) of the MEP and CMAPs were investigated. These potentials were generated by stimulation of the spinal cord and the motor cortex, respectively. Enflurane (2%), halothane (1%) and isoflurane (1.5%) with pure oxygen decreased the amplitude of the I wave to less than 50% of the control level. The CMAP after stimulation of the spinal cord was degraded to less than 30%, and the CMAP after cortical stimulation vanished completely. Only the D wave was stable against inhalational anesthetic agents. Sixty-seven percent nitrous oxide with the above concentrations of these inhalational anesthetic agents decreased the amplitude of the I wave to less than 30% and the CMAP evoked by spinal cord stimulation vanished. The effect of modified NLA (diazepam and pentazocine) on these potentials was weaker than that of the inhalational anesthetic agents.

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PubMed1997

[Myocardial cells action potential and contractive function in hemorrhagic shock in rabbits].

Anesthetized rabbits were subjected to a moderate degree of hemorrhagic shock. Lowering their mean arterial pressure to 5.3 KPa for 3 h, we measured the mean arterial pressure (MBP), left ventricular systolic pressure (LVSP), left ventricular maximum velocities of contraction (dp/dtmax), and myocardial electrical activity. The results of this study demonstrated that LVSP declined in parallel with MBP; that dp/dtmax dropped acutely on the instant of hemorrhagic shock; dp/dtmax went up by 48% on 15 min after shock; then dp/dtmax fell gradually, and by 3 h after shock the dp/dtmax values dropped to 20% of the baseline values; that intracellular sodium and potassium contents increased significantly in the hemorrhagic shocked rabbits; that myocardial resting potential (RP) and action potential amplitude (APH) diminished; and that action potential duration(APD), action potential repolarized 50% duration (APD 50), and repolarized 90% duration (APD 90) were markedly prolonged in the hemorrhagic shock, compared with control. The results suggested that in hemorrhagic shock myocardial cells fast sodium channel was closed while slow sodium and slow calcium channels, were opened; thus sodium and calcium infused and potassium exuded.

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PubMed1981

The effects of heart rate on the action potential of guinea-pig and human ventricular muscle.

1. On increasing the stimulation frequency of isolated pieces of guinea-pig ventricular muscle, the resting potential depolarizes, and the action potential duration and amplitude are reduced. On termination of the high frequency train of action potentials, these changes are reversed. 2. The resting potential changes are roughly exponential, with a time constant of the order of 10 sec, and are attributable to K+ accumulation in the extracellular space. They are not explicable in terms of known gating variables. 3. The action potential duration and amplitude recover much more slowly than the resting potential, after a high frequency train (half-time approximately 5 min). The time course of these recoveries is not exponential, and is slower after trains which produce more shortening of the action potential. The slow time course suggests that K+ accumulation is not the main cause of the changes in action potential shape. Furthermore, when a certain depolarization of the resting potential is produced by a high frequency train, there is a greater reduction of the action potential duration than that which occurs when the bathing [K+] is raised to produce the same depolarization (Reiter & Stickel, 1968). This is so even when a gradient of extracellular [K+] is induced in the preparation, to mimic non-uniform K+ accumulation. 4. Similarly, the shortening of the action potential produced by toxic doses or cardiotonic steroids is probably not the result of K+ accumulation. 5. The slow changes of the action potential shape produced by a high frequency train are not attributable to the effects of gating variables, nor (solely) to a rise in the intracellular Na concentration stimulating the electrogenic Na/K pump. The dye 3,3'-diethylthiadicarbocyanine, which blocks the Ca2+-activated K conductance in the erythrocyte, has no significant effect on the shape changes. 6. After a sudden change in heart rate, the QT interval of the human electrocardiogram (e.c.g.) changes slowly to a new equilibrium value. The time course of this change is similar to that of the action potential duration in guinea-pig ventricle following a change in stimulation frequency. These changes of the e.c.g. are probably not due to slow alterations of neural or hormonal factors extrinsic to the heart. In the whole heart, the effects on the ventricular action potential duration of changes in sympathetic or vagal tone, or of circulating catecholamines, can be largely accounted for by the changes of atrial driving frequency they produce.

Action Potentials↗
PubMed1976

Phase-plane analysis of action potentials in uterine smooth muscle.

Action potentials were recorded by microelectrode from narrow strips of pregnant rat uterus in vitro. The phase-plane display (V vs dV/dt) of selected action potentials was analysed by the method of Jenerick (1964) to yield the ionic current. From this membrane current data, various parameters of the action potential were calculated. In comparison to skeletal muscle action potentials, the ionic currents were 30-100 times smaller in the uterus action potential. Epinephrine hyperpolarized the resting potentials and suppressed spontaneous activity, but did not cause any significant changes in the stimulated action potential. The after-potential may have been affected by epinephrine, preventing repetitive firing, but the data were inconclusive. The phase-plane analysis results were similar to the results of the double sucrose gap voltage clamp method on the same tissue (Kao and McCullough, 1975).

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PubMed2002

[Monophasic action potentials: considerations and limits].

Monophasic action potentials are currents recorded in vivo in the extracellular milieu which can reproduce the repolarisation signal of intracellular action potentials. For a long time unstable and complex to record, they now require simply a firm myocardial contact with a bipolar electrophysiological catheter and modification with recording filters, without a high-pass filter (DC). They have been widely used in recent years to study in vivo modifications of the action potential durations with frequency, epi-, endo-, or intramyocardial cellular topography, endocavity pressure modifications, or antiarrhythmic medication. They allow a unique means of continuous analysis in animals or in patients of the action potentials during polymorphic arrhythmias such as atrial fibrillation, ventricular fibrillation and torsades de pointes, although in these cases the refractory periods can not be measured precisely and continuously, beat after beat. In contrast, their clinical or experimental use in the study of arrhythmias dependent on premature post-depolarisations has without doubt been excessive and disputable, because it appears improbable that authentic premature post-depolarisations could ever be obtained on a monophasic action potential, which always represents the summation of the action potentials of dozens of cells.

Action Potentials↗
PubMedDate not supplied

Oscillations of cytosolic Ca2+ in pituitary cells due to action potentials.

Electrical activity in non-neuronal cells can be induced by altering the membrane potential and eliciting action potentials. For example, hormones, nutrients and neurotransmitters act on excitable endocrine cells. In an attempt to correlate such electrical activity with regulation of cell activation, we report here direct measurements of cytosolic free Ca2+ changes coincident with action potentials. This was achieved by the powerful and novel combination of two complex techniques, the patch clamp and microfluorimetry using fura 2 methodology. Changes in intracellular calcium concentration were monitored in single cells of the pituitary line GH3B6. We show that a single action potential leads to a marked transient increase in cytosolic free calcium. The size of these short-lived maxima is sufficient to evoke secretory activity. The striking kinetic features of these transients enabled us to identify oscillations in intracellular calcium concentration in unperturbed cells resulting from spontaneous action potentials, and hence provide an explanation for basal secretory activity. Somatostatin, an inhibitor of pituitary function, abolishes the spontaneous spiking of free cytosolic Ca2+ which may explain its inhibitory effect on basal prolactin secretion. Our data therefore demonstrate that electrical activity can stimulate Ca2+-dependent functions in excitable non-neuronal cells.

Action Potentials↗
PubMed1990

Mechanism of potassium efflux and action potential shortening during ischaemia in isolated mammalian cardiac muscle.

1. Ischaemia was simulated in the isolated sheep cardiac Purkinje fibre and guinea-pig papillary muscle by immersing the preparations in paraffin oil. Ion-selective microelectrodes recorded potassium (Ks+) and pH (pHs) in the thin film of Tyrode solution trapped at the fibre surface while other microelectrodes recorded intracellular pH (pHi), membrane potential and action potentials (AP) (evoked by field stimulation), or membrane current (two-microelectrode voltage clamp in shortened Purkinje fibres). Twitch tension was also monitored. The paraffin oil model reproduced the salient characteristics of myocardial ischaemia, i.e. a decrease of twitch tension; a decrease of pHi and pHs; a rise in Ks+ (by 2-3 mM); a depolarization of diastolic membrane potential; considerable shortening of the AP (up to 30% within 4 min). 2. The sulphonylurea compounds, glibenclamide (200 microM) and tolbutamide (1 mM), known inhibitors of the KATP channel, completely blocked the ischaemic rise of Ks+ and prevented AP shortening. Ischaemic tension decline was notably less pronounced in the presence of sulphonylureas. 3. The ischaemic increase of slope conductance (Purkinje fibre) was prevented by 1 mM-tolbutamide and 200 microM-glibenclamide. 4. Sulphonylureas did not affect resting membrane potential, the AP or the current-voltage relationship under non-ischaemic conditions (this also indicates that ischaemic Ks+ accumulation is not fuelled by the background K+ current [iK1] which was shown, as expected, to be Ba2+ sensitive). 5. In a normally perfused preparation, reducing intracellular ATP by inhibiting glycolysis with 2-deoxyglucose (DOG) produced a similar AP shortening plus a membrane hyperpolarization, both of which were inhibited by tolbutamide or glibenclamide. The AP shortening was not related uniquely to the fall of pHi observed under these conditions since experimentally reducing pHi (by reducing pHo in the absence of DOG) lengthened rather than shortened the AP. 6. The possibility that the ischaemic rise in Ks+ might be the cause of AP shortening was excluded by the observation that, in a normally perfused Purkinje fibre, experimentally reducing pHi (by an amount similar to that seen during ischaemia) completely neutralized the AP-shortening effect of an elevated Ko+ (from 4.5 to 6.5 mM). Furthermore, the sulphonylurea-sensitive AP shortening seen during DOG treatment could not have been associated with a Ks+ rise since, in these particular experiments, the fibres were well perfused and diastolic membrane potential hyperpolarized.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2005

Two-photon excitation of di-4-ANEPPS for optical recording of action potentials in rabbit heart.

Cardiac action potentials have been measured with single-photon excitation (SPE) of transmembrane voltage-sensitive fluorescent dye. Two-photon excitation (TPE) may have advantages for localization and depth of the tissue region from which the action potential is measured. However measurements of action potentials with SPE have not been demonstrated. We sought to develop a method for TPE of di-4-ANEPPS and test whether the method yields voltage-dependent fluorescence in cardiac tissue. We modified our SPE and ratio-metric fluorescence recording system to use a femtosecond pulsed near-infrared laser. Modifications were made to enhance fluorescence collection efficiency and to block infrared laser light from entering the fluorescence collection system. Fluorescence was collected simultaneously in green (510-570 nm) and red (590-700 nm) wavelength bands. Action potentials were observed in the ratio of the green signal to the red signal, but were not observed above the noise level in either of the individual signals. Incorporation of a common-mode noise subtraction method revealed action potentials in green and red signals. We also found that the di-4-ANEPPS fluorescence emission spectrum for TPE at 930 nm was similar to the emission spectrum for SPE at 488 nm. The multiphoton method may be beneficial for highly localized cardiac optical measurements.

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PubMed2005

Compensation of intraoperative transcranial motor-evoked potential monitoring by compound muscle action potential after peripheral nerve stimulation.

It is often difficult to evaluate the results of transcranial motor-evoked potential (TCMEP) monitoring in patients under general anesthesia because these results are strongly affected by anesthetics and muscle relaxants. To exclude effects of muscle relaxants on TCMEP, compound muscle action potential (CMAP) by supramaximum stimulation of the median nerve immediately after transcranial stimulation (300 to 600 V) was recorded in 70 neurosurgical operations. A relative amplitude index (RAI) was defined as the amplitude of TCMEP after the operative procedure divided by the amplitude of TCMEP before the operative procedure. The RAI was calculated and was compensated by the amplitude of CMAP in 141 limbs. In 12 limbs of 7 patients with postoperatively progressed motor paresis, the compensated RAI was less than 0.2. The compensated RAI in all other 129 limbs of 63 patients without postoperative motor palsy was more than 0.2. These results suggest that compensation of TCMEP monitoring by CMAP is an easy and accurate method for removing the effects of muscle relaxants in TCMEP.

Action Potentials↗
PubMed1994

Prolongation by captopril of action potential duration in the normal and hypertrophied rat ventricle: direct action or inhibition of the local angiotensin converting enzyme?

OBJECTIVE: The aims were: (1) to study the acute effects of captopril on the action potential characteristics of ventricular fibres from the normal rat, (2) to compare the effects of captopril with those of perindoprilat, a non-thiol angiotensin I converting enzyme (ACE) inhibitor, (3) to determine the electrophysiological properties of the peptide substrates of converting enzyme, bradykinin and angiotensin I, and (4) to investigate whether the effects of captopril occurring in the healthy heart also occur in two models of ventricular hypertrophy. METHODS: Action potentials were recorded with the standard glass microelectrode technique in right ventricular preparations excised from rat hearts and superfused under baseline conditions and with drug containing or peptide containing Tyrode solution. Ventricular hypertrophy was induced in response to hypertension (unilaterally nephrectomised, DOCA-salt model) or 4 week old left ventricular infarction. RESULTS: In preparations from normal rat hearts, captopril increased action potential duration in a concentration dependent fashion [EC50 = 3.5 x 10(-8) M; maximum effect = 44(SEM 5.1)% prolongation at 10(-5) M for action potential duration at 90% repolarisation, APD90]. Perindoprilat similarly caused a dose dependent increase in action potential duration, but with 100 times greater potency [EC50 = 3.1 x 10(-10) M; maximum effect = 71(11)% prolongation at 10(-5) M for APD90]. SQ 14,534, a stereoisomer of captopril with one hundredth the ACE inhibitor potency, had no significant effect on action potential duration at 10(-5) M. Angiotensin I and bradykinin caused concentration dependent prolongation of action potential, but angiotensin II (10(-6) M) had no effect. Captopril (10(-5) M) had no significant effect in the hypertrophied right ventricle from DOCA-salt hypertensive rats, but significantly increased APD90 [39(4.9)%] in right ventricular preparations from rats with 4 week old anterior left ventricular infarction. CONCLUSIONS: In the rat, captopril prolongs action potential duration, an effect possibly due to local accumulation of bradykinin and angiotensin I.

Action Potentials↗
PubMed2005

Stimulus history reliably shapes action potential waveforms of cortical neurons.

Action potentials have been shown to shunt synaptic charge to a degree that depends on their waveform. In this way, they participate in synaptic integration, and thus in the probability of generating succeeding action potentials, in a shape-dependent way. Here we test whether the different action potential waveforms produced during dynamical stimulation in a single cortical neuron carry information about the conductance stimulus history. When pyramidal neurons in rat visual cortex were driven by a conductance stimulus that resembles natural synaptic input, somatic action potential waveforms showed a large variability that reliably signaled the history of the input for up to 50 ms before the spike. The correlation between stimulus history and action potential waveforms had low noise, resulting in information rates that were three to four times larger than for the instantaneous spike rate. The reliable correlation between stimulus history and spike waveforms then acts as a local encoding at the single-cell level. It also directly affects neuronal communication as different waveforms influence the production of succeeding spikes via differential shunting of synaptic charge. Modeling was used to show that slow conductances can implement memory of the stimulus history in cortical neurons, encoding this information in the spike shape.

Action Potentials↗
PubMed1998

[Comparison between selenomethionine and sodium selenite on action potentials of cultured myocardiocytes].

The action potentials of ventricular myocardial cells were recorded with glass microelectrodes inside the cells from neonatal Wistar rats treated with selenomethionine and sodium selenite in concentrations of 1.0, 2.0, and 4.0 mg/L selenium. Both of selenomethionine and sodium selenite decreased the action potential parameters, such as action potential amplitude(APA), overshoot(OS), threshold potential(TP), maximum diastolic potential (MDP) and maximum rate of depolarization (Vmax). Selenomethionine decreased the action potential duration at 10%, 50% and 90% repolarization (APD10, APD50 and APD90), while sodium selenite prolonged APD10, APD50 and APD90 at dose of 4.0 mg/L selenium and decreased APD50 and APD90 at dose of 1.0 and 2.0 mg/L selenium. The results indicated that both sodium selenite and selenomethionine inhibit the transmembrane movement of Ca2- and sodium selenite also inhibits transmembrane movement of K+.

Action Potentials↗
PubMed1999

Electrophysiological basis of mono-phasic action potential recordings.

Monophasic action potentials (MAPs) have been recorded for over a century, however, the exact mechanism responsible for their genesis has yet to be elucidated fully. The goal of the paper is to examine the physical basis of MAP recordings. MAP recordings are simulated by modelling a three-dimensional block of cardiac tissue. The effect of the MAP electrode is modelled by introducing a large, non-specific leakage conductance to the small region under the electrode. From the spread of the electrical activity, the equivalent extracellular current flow can be efficiently determined. These computed current sources are then input into a boundary element model of the tissue to determine the surface potentials. Finally, differences in surface potentials are used to compute waveforms that closely resemble MAP recordings. By varying model parameters, the mechanisms responsible for the MAP are determined, and a theory is put forward that can account for all observations. It is hypothesised that the leakage current causes the formation of a double-layer potential with a strength equal to the difference in transmembrane voltage between the regions under the electrode and those outside the electrode, leading to a recorded potential that mimics the transmembrane voltage outside the electrode region, although offset. Based on experimental MAP recordings, an equivalent leakage channel with a conductance of 0.1 mS cm-2 and a reversal potential of -43 mV is introduced by the electrode.

Action Potentials↗
PubMed1977

[Analysis of action potentials of muscles by a small general purpose computer (author's transl)].

To measure the duration of action potentials by a computer, the following steps are necessary: 1. automatic selection of suitable potentials from the EMG 2. identification of equal potentials (action potentials of the single motor unit) 3. measuring the durations of potentials, defined by the distance between first and last deviation from the base line. We noticed that the automatic evaluation of durations of single potentials is greatly deteriorated by base-line fluctuations. Therefore we average about 16 action potentials, stored in the computer, of the same single motor unit and measure the duration of the averaged potential.

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