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PubMed1978

An analysis of the effect of the rate of stimulation and adrenaline on the duration of the cardiac action potential.

1. Changes of action potential duration in cat papillary muscle have been correlated with changes of peak tension. It has been assumed that peak tension is an approximate indicator of [Ca2+]i. 2. When stimulation is commenced after a rest of several minutes, or after a decrease or increase of the stimulus rate, or after rest periods of different duration the changes of action potential duration are closely related to changes of peak tension. These results suggest that [Ca2+]i is of primary importance in determining rate-dependent changes of action potential duration, including the shortening of the action potential at high rates of stimulation. 3. The results also indicate the presence of a factor which tends to prolong the action potential at high rates of stimulation. Thus the duration of the action potential at high stimulus rates is longer than at lower rates when measured at a given value of peak tension. Furthermore in low Ca2+ there can be a prolongation of the steady state action potential at high rates. Comparison with the work of Cohen et al. (1976) suggests that this factor is responsible for the polarity of the T-wave of the ECG. 4. The action of adrenaline on action potential duration has also been analysed. It is shown to have two effects--a prolonging effect probably related to the adrenaline induced increase of Isi, and a shortening effect probably related to an increase of [Ca2+]i (as judged by the increase of peak tension).

Action Potentials↗
PubMed1994

Kappa-selective agonists decrease postsynaptic potentials and calcium components of action potentials in the supraoptic nucleus of rat hypothalamus in vitro.

To investigate the effects of the endogenous kappa-receptor agonists dynorphin and leumorphin on neurons of the supraoptic nucleus in the rat hypothalamus, intracellular recordings were made from 62 supraoptic neurons in slice preparations. Bath application of dynorphin and leumorphin at 10(-7) M to 3 x 10(-6) M decreased the spontaneous firing rate with slight hyperpolarization of the membrane potential (-3.8 +/- 0.5 mV, mean +/- S.E.M.) but did not detectably change input resistance. The inhibitory effects were blocked by the relatively selective kappa-antagonist MR-2266. The synthetic kappa-receptor agonist U-50,488H had similar inhibitory effects on supraoptic neurons. Postsynaptic potentials evoked by electrical stimulation dorsal or dorsolateral to the supraoptic nucleus were suppressed by dynorphin and leumorphin. Morphine and [D-Ala, D-Leu]enkephalin, which are relatively selective to mu- and delta-receptors, respectively, influenced the postsynaptic potentials less. Dynorphin and leumorphin also decreased the duration of action potentials that were prolonged by either bath application of tetraethylammonium chloride at 5-10 mM or intracellular injection of Cs ions from the recording electrodes which were filled with 3 M cesium citrate. The prolongation was blocked by 1 mM MnCl2 and 2 mM CoCl2, which suggested that the components were due to voltage-dependent Ca2+ influx. The results suggest that endogenous kappa-receptor agonists inhibit neurosecretory cells of the supraoptic nucleus to suppress synaptic events and Ca2+ components of action potentials.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1989

Mechanism of potentiation of contraction by depolarization during action potentials in guinea-pig ventricular muscle.

Action potentials were recorded from guinea-pig ventricular cells and contraction recorded by an optical technique. When the plateau of a single action potential was depolarized (by 70-120 pA applied 100 ms after the upstroke for 100 ms), contraction associated with the following normal action potential was potentiated. This potentiation was not seen in cells exposed to 10 mM-caffeine. The observations are consistent with potentiation of subsequent contraction by increased loading of caffeine-sensitive calcium stores, as a consequence of reduced Ca2+ extrusion or possibly Ca2+ entry via Na+-Ca2+ exchange during a depolarized plateau.

Action Potentials↗
PubMed2000

Preceding stimulus frequency-dependent potentiation of the postrest shortening of the action potential duration in rabbits.

Action potential duration (APD) in rabbit ventricular myocardium shortens after a rest period (postrest shortening). However, the effects of preceding stimulus frequency on the postrest shortening have not been elucidated. We recorded transmembrane action potentials (TAPs) and monophasic action potentials (MAPs) from the rabbit ventricle. In in vitro experiments. repetitive regular stimuli (S1) at cycle lengths ranging between 500 to 3000 ms were followed by a single extrastimulus (S2) at a coupling interval of 5000 ms. A decrease in S1S1 interval resulted in a progressive shortening of the duration of TAP (TAPD) elicited by S2 (S2-TAPD), which was potentiated by increasing extracellular calcium concentration ([Ca2+]o) or application of ouabain and was inhibited by lowering [Ca2+]o or verapamil. Application of ryanodine was most effective in lengthening S2-TAPD following a short S1S1 interval. 4-aminopyridine and E4031 caused marked lengthening of S2-TAPD when S1S1 was long. However, the lengthening effect was attenuated and disappeared with a shorter S1S1 interval. In in vivo experiments, regular ventricular pacing (S1) at cycle lengths ranging between 250 to 1000 ms was followed by a single extrastimulus (S2) with a coupling interval (S1S2) of 1500 ms. A decrease in the S1S1 interval also resulted in progressive shortening of the duration of MAP elicited by S2. Our results indicate that the postrest shortening is potentiated by an increase in the preceding stimulus frequency in the rabbit ventricle, in which the function of sarcoplasmic reticulum may play a significant role.

Action Potentials↗
PubMed2005

A MULTICHANNEL FIBER-OPTIC MAPPING SYSTEM FOR INTRAMURAL RECORDING OF CARDIAC ACTION POTENTIALS.

Measuring cardiac action potentials at many sites within the ventricular wall is important for understanding cardiac arrhythmias; however, recording in the depth of the heart wall presents many difficulties. We have developed a multichannel optical mapping system for recording cardiac action potentials transmurally. Each channel uses a single small-diameter optical fiber to transmit and collect light from the cardiac tissue. Excitation light is supplied by low-power green lasers. Wavelength separation is performed with a dichroic mirror, and fluorescence is detected with a photodiode. We have recorded action potentials with an unfiltered signal-to-noise ratio (SNR) as high as 60:1 and a temporally filtered SNR as high as 200:1. The collection of fluorescence is optimized so that low excitation light intensity can be used, which increases the available recording time. Channels are modular and compact, and the system can be easily expanded to include additional channels, ratiometry or dual-dye mapping. In addition, the system is highly flexible and can be used for virtually any experiment from single cell recording to surface and transmural mapping of the whole heart.

Journal Article↗
PubMed1990

Chloride current in mammalian cardiac myocytes. Novel mechanism for autonomic regulation of action potential duration and resting membrane potential.

The properties of the autonomically regulated chloride current (ICl) were studied in isolated guinea pig ventricular myocytes. This current was elicited upon exposure to isoproterenol (ISO) and reversed upon concurrent exposure to acetylcholine (ACh). ICl was time independent and exhibited outward rectification. The responses to ISO and ACh could be blocked by propranolol and atropine, respectively, and ICl was also elicited by forskolin, 8-bromoadenosine 3',5'-cyclic monophosphate, and 3-isobutyl-l-methylxanthine, indicating that the current is regulated through a cAMP-dependent pathway. The reversal potential of the ISO-induced current followed the predicted chloride equilibrium potential, consistent with it being carried predominantly by Cl-. Activation of ICl produced changes in the resting membrane potential and action potential duration, which were Cl- gradient dependent. These results indicate that under physiological conditions ICl may play an important role in regulating action potential duration and resting membrane potential in mammalian cardiac myocytes.

Acetylcholine↗
PubMed1985

Effect of higenamine on action potential of ventricular myocardial cells.

Action potentials of isolated ventricular myocardial fibers of pigs and the electrophysiological actions of dl-demethylcoclaurine (DMC) or higenamine on the porcine myocardial cells were studied by glass microelectrodes. The action potentials of porcine ventricular myocardial fibers were similar to those of other mammalian hearts. Amplitude of the action potential was 115 +/- 9 mV, duration of action potential 242 +/- 30 ms, resting membrane potential -85 +/- 5 mV and the maximum rise of depolarization of action potential 151 +/- 27 V/s. After perfusion with normal Tyrode's solution containing DMC 5 micrograms/ml, the amplitude of action potential was increased and the duration of action potential was prolonged, the amplitude and duration of the plateau of action potential were increased and the slope of phase 2 of action potential was reduced (p less than 0.05). The resting potential, the slope of phase 3 and the maximum depolarization rate of phase 0 of action potential did not change. In Tyrode's solution containing Mn++ 3 mM, these electrophysiological actions of DMC disappeared. DMC may abolish the conduction block induced by K+-rich solution. In Tyrode's solution containing K+ 32 mM, the upstroke of action potential showed 2 phases under influence of DMC. The second phase disappeared when Mn++ was added. All findings indicate that DMC can be considered as an activator of the slow channel. The electrophysiological mechanism and clinical significance of DMC were discussed.

Alkaloids↗
PubMed2004

Ionic mechanisms in the generation of subthreshold oscillations and action potential clustering in entorhinal layer II stellate neurons.

A multicompartmental biophysical model of entorhinal cortex layer II stellate cells was developed to analyze the ionic basis of physiological properties, such as subthreshold membrane potential oscillations, action potential clustering, and the medium afterhyperpolarization. In particular, the simulation illustrates the interaction of the persistent sodium current (I(Nap)) and the hyperpolarization activated inward current (Ih) in the generation of subthreshold membrane potential oscillations. The potential role of Ih in contributing to the medium hyperpolarization (mAHP) and rebound spiking was studied. The role of Ih and the slow calcium-activated potassium current Ikappa(AHP) in action potential clustering was also studied. Representations of Ih and I(Nap) were developed with parameters based on voltage-clamp data from whole-cell patch and single channel recordings of stellate cells (Dickson et al., J Neurophysiol 83:2562-2579, 2000; Magistretti and Alonso, J Gen Physiol 114:491-509, 1999; Magistretti et al., J Physiol 521:629-636, 1999a; J Neurosci 19:7334-7341, 1999b). These currents interacted to generate robust subthreshold membrane potentials with amplitude and frequency corresponding to data observed in the whole cell patch recordings. The model was also able to account for effects of pharmacological manipulations, including blockade of Ih with ZD7288, partial blockade with cesium, and the influence of barium on oscillations. In a model with a wider range of currents, the transition from oscillations to single spiking, to spike clustering, and finally tonic firing could be replicated. In agreement with experiment, blockade of calcium channels in the model strongly reduced clustering. In the voltage interval during which no data are available, the model predicts that the slow component of Ih does not follow the fast component down to very short time constants. The model also predicts that the fast component of Ih is responsible for the involvement in the generation of subthreshold oscillations, and the slow component dominates in the generation of spike clusters.

Action Potentials↗
PubMed1996

Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure.

Membrane current abnormalities have been described in human heart failure. To determine whether similar current changes are observed in a large animal model of heart failure, we studied dogs with pacing-induced cardiomyopathy. Myocytes isolated from the midmyocardium of 13 dogs with heart failure induced by 3 to 4 weeks of rapid ventricular pacing and from 16 nonpaced control dogs did not differ in cell surface area or resting membrane potential. Nevertheless, action potential duration (APD) was significantly prolonged in myocytes isolated from failing ventricles (APD at 90% repolarization, 1097 +/- 73 milliseconds [failing hearts, n = 30] versus 842 +/- 56 milliseconds [control hearts, n = 25]; P < .05), and the prominent repolarizing notch in phase 1 was dramatically attenuated. Basal L-type Ca2+ current and whole-cell Na+ current did not differ in cells from failing and from control hearts, but significant differences in K+ currents were observed. The density of the inward rectifier K+ current (IKl) was reduced in cells from failing hearts at test potentials below -90 mV (at -150 mV, -19.1 +/- 2.2 pA/pF [failing hearts, n = 18] versus -32.2 +/- 5.1 pA/pF [control hearts, n = 15]; P < .05). The small outward current component of IKl was also reduced in cells from failing hearts (at -60 mV, 1.7 +/- 0.2 pA/pF [failing hearts] versus 2.5 +/- 0.2 pA/pF [control hearts]; P < .05). The peak of the Ca(2+)-independent transient outward current (Ito) was dramatically reduced in myocytes isolated from failing hearts compared with nonfailing control hearts (at +80 mV, 7.0 +/- 0.9 pA/pF [failing hearts, n = 20] versus 20.4 +/- 3.2 pA/pF [control hearts, n = 15]; P < .001), while the steady state component was unchanged. There were no significant differences in Ito kinetics or single-channel conductance. A reduction in the number of functional Ito channels was demonstrated by nonstationary fluctuation analysis (0.4 +/- 0.03 channels per square micrometer [failing hearts, n = 5] versus 1.2 +/- 0.1 channels per square micrometer [control hearts, n = 3]; P < .001). Pharmacological reduction of Ito by 4-aminopyridine in control myocytes decreased the notch amplitude and prolonged the APD. Current clamp-release experiments in which current was injected for 8 milliseconds to reproduce the notch sufficed to shorten the APD significantly in cells from failing hearts. These data support the hypothesis that downregulation of Ito in pacing-induced heart failure is at least partially responsible for the action potential prolongation. Because the repolarization abnormalities mimic those in cells isolated from failing human ventricular myocardium, canine pacing-induced cardiomyopathy may provide insights into the development of repolarization abnormalities and the mechanisms of sudden death in patients with heart failure.

Action Potentials↗
PubMed1988

Somatostatin blocks Ca2+ action potential activity in prolactin-secreting pituitary tumor cells through coordinate actions on K+ and Ca2+ conductances.

The hypothalamic peptide somatostatin (SRIF) suppresses secretory activity in phenotypically distinct pituitary endocrine cells. We have used tight-seal whole-cell recording techniques to study the peptide's effects on the electrical properties of tumor pituitary cells derived from rat (GH3/B6) and human adenomas that secrete human PRL in a SRIF-sensitive manner. Both cell types exhibited qualitatively similar electrophysiological properties and electrical responses to SRIF. Under the experimental conditions employed the majority of cells spontaneously generated Ca2+-dependent actions potentials. The actions of the peptide on cellular excitability were markedly affected by the presence of horse and fetal calf sera. Without these additives the electrical responses faded and could not be studied in detail. Therefore, recordings were conducted in media containing sera. In the presence of sera almost all cells spontaneously generated Ca2+ action potentials, and peptide-induced changes in excitability were well preserved. SRIF depressed spontaneous and evoked action potential activity in a dose-dependent manner at concentrations that reduced intracellular free calcium ([Ca2+]i) and suppressed basal PRL release. Current and voltage clamp experiments revealed coordinate actions of the peptide on excitable membrane properties. SRIF (1 nM) enhanced a depolarization-activated, rapidly inactivating outward K+ current, thereby effectively reducing the rate at which action potentials occurred. Over the 10-1000 nM range SRIF slowly activated a virtually noninactivating K+ conductance over a wide range of membrane potential. This effectively hyperpolarized cells away from the threshold for triggering Ca2+-dependent action potentials and shunted the membrane. The peptide induced K+ conductance activated at the level of the resting potential was progressively lost during the intracellular dialysis of whole-cell recording. Dilute aqueous lysates of cells included in the patch pipette prevented much of the rundown of this SRIF-induced electrical response while inclusion of an ATP-regenerating system preserved some of the peptide action. Over the 10-100 nM concentration range SRIF also reduced voltage-dependent Ca2+ current. Furthermore, pretreatment of cells with pertussis toxin abolished SRIF action on cellular excitability, suggesting that SRIF can regulate the function of ionic channels through GTP-binding proteins (G proteins). The results demonstrate that SRIF acts coordinately on the primary conductances expressed in tumor PRL cells to attenuate or block Ca2+ action potential generation and thus Ga2+ entry from extracellular sources.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMedDate not supplied

Computer simulation study of the shape of motor unit action potential.

Motor unit action potentials (MUAPs) of brachial biceps were simulated. A simulated MUAP was obtained as a sum of single fibre action potentials (SFAPs) from all the muscle fibres of a motor unit (MU). The influence of the following factors on MUAP shape for different kinds of recording electrode was studied: fibre density, neuromuscular jitter, temporal dispersion and electrode displacements. The simulation confirms that typical MUAPs recorded with needle electrodes from muscles of low fibre density such as brachial biceps are usually triphasic. Increased fibre density produces MUAPs of more complex shape and higher amplitude. Normal neuromuscular jitter is responsible for the variability of shape of subsequent potentials from the same MU as well as for electromyographic shimmer. Pathologic (increased) jitter makes the shapes of subsequent potentials unrecognizable. The influence of temporal dispersion is interconnected with other factors but rather of minor importance. The simulation shows how big changes in MUAP shape can be expected due to electrode displacements during single experiment or during estimation of MU territory.

Action Potentials↗
PubMed1995

[Stimulus effect and jumping of delayed potentials--investigation of human single nerve action potentials].

The jumping phenomenon is defined as an unexpected reduction in latency of evoked nerve responses with augmentation of stimulus intensity. This phenomenon may occur in the presence of segmental demyelination. To determine the severity of neuropathies, we recorded median nerve action potentials at the elbow of 60 patients of neuropathy by means of intraneural microneurography. Submaximal stimuli were delivered at the wrist or at one finger. In 53 of the 60 patients evaluated, delayed single nerve action potentials were recorded by submaximal stimuli that produced less than 10 microV compound nerve action potentials. In three delayed single unit potentials, latencies were shortened unexpectedly by several milliseconds when the intensity of stimulus was gradually increased. With the boundary stimulus intensity, we observed a small amplitude of the corresponding potentials at the delayed and the jumped latencies. Instead, jumping was suppressed with rapid repetitive stimuli. At the stimulus intensity sufficient to provoke jumping, we administered repetitive stimuli at 2Hz to 50Hz. At the rate of 20 to 30Hz, the corresponding potentials again returned to the delayed latencies. Rapid repetitive impulses may evoke cathodal hyperpolarization which raises the excitation threshold of the nerve. Thus, the stimulus effect can be decreased and jumping will be released. In addition, a diminution in amplitude and slight prolongation of the latency of each peak occurred in proportion to the increase in stimulus rate. However, paired stimuli with an interval of 4 to 13 msec was equivalent to a supernormal period and provoked the jumping of a single nerve unit. Conditioning stimuli may have increased the excitability of the corresponding fiber.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1989

Principal component analysis of the features of concentric needle EMG motor unit action potentials.

Motor unit action potentials (MUAPs) were recorded from the biceps muscle of normal subjects and of patients with nerve or muscle diseases. Principal component analysis of the MUAP amplitude, area, area/amplitude ratio, duration, and the number of turns and phases produced three components that among them contained 90% of the variance of the data set. Thus the dimensionality of data was reduced from six to three. The first component reflected changes in the size of the MU, whereas the second reflected variations in the arrival time at the recording electrode of the action potentials of muscle fibers in the motor unit. The third factor reflected local loss of muscle fibers within the MU territory. Patterns of variations in the three components were different in patients with neuropathy and myopathy.

Action Potentials↗
PubMed1991

The recording of action potential currents as an assessment for drug actions on excitable cells.

The use of the cell-attached patch clamp configuration to record action potential currents is shown to have utility in the testing for drug actions on ion channels in excitable cell membrane. A patch pipette was used to isolate a small patch of cell membrane on cultured hippocampal or hypothalamic neurons and spontaneous R-C coupled action potential currents, with well-defined Na+ and K+ components, were recorded. The addition of several potassium channel-blocking drugs to the bath solution completely abolished the after-hyperpolarization phase of the action potential currents while preserving the sodium spike. These drugs have previously been shown to block a calcium-dependent potassium channel in cultured hippocampal neurons, a channel that is responsible for the late slow after-hyperpolarization macroscopic current recorded in these cells. The addition of tetrodotoxin to the bath solution eliminated the R-C coupled currents. The novel approach of using the recording of action potential currents to assess drug actions on ion channels would be expected to be applicable to a variety of excitable cells.

Action Potentials↗