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At least 163 records · Page 9Linked to original sources
PubMed1981

Dual influence of temperature on compound nerve action potential.

Compound neural action potentials (NAPs) were recorded from N. suralis and the digital nerves of N. medianus in man using the antidromic technique. The nerves were cooled either at the site of the recording ("local cooling") avoiding temperature change proximally, or between the stimulating and recording electrodes ("segmental cooling") avoiding temperature change at the recording site. Local cooling was followed by a pronounced increase in NAP amplitude and rise time without any change in the onset latency. The values of Q10 were identical for both amplitude and rise time changes. Segmental cooling caused a definite fall in the amplitude of NAP and a slight increase in its rise time. The practical consequences of the dual temperature effect on NAP are discussed.

Action Potentials↗
PubMed1970

Modification of transmitter release by ions which prolong the presynaptic action potential.

1. The action of ions which increase the nerve spike duration at Ranvier's node has been studied at the neuromuscular junction of the frog.The duration of the presynaptic action potential is increased by UO(2), Ni, Nz and TEA ions.2. The release of transmitter after a nerve impulse is delayed and prolonged in the presence of the four ions, but the amount of evoked transmitter release estimated from the mean quantal content of e.p.p. is increased only by UO(2) (2+) and TEA. Both Ni(2+) and Zn(2+) decrease it.3. The frequency of m.e.p.p.s is increased by UO(2) (2+) and decreased by Ni(2+) and Zn(2+) at KCl-depolarized junctions. It is not affected by TEA.4. It has been concluded that the increased presynaptic spike duration is responsible for the delayed and prolonged transmitter release in the presence of ions which increase the nerve spike duration at Ranvier's node. It is demonstrated that some ;specific' effects possibly resulting from ionic competition for presynaptic sites between UO(2) (2+), Ni(2+) or Zn(2+) and other ions present in the Ringer may increase, interfere with, or hide the increased transmitter release that may be predicted from the lengthened presynaptic depolarization.

Action Potentials↗
PubMed1985

[Electric activation of the heart using laser spectrometry. 1. Study of transmembrane action potentials using optical technics].

The action potentials of the contractile myocardium and conduction cells are usually recorded by intracellular glass microelectrodes but they call also be obtained at a distance and without physical contact by optical techniques. The myocardial fragment must be stained with a dye which, when illuminated by a laser beam, emits a fluorescence whose wave length is related to the transmembrane potential. The responses obtained were checked by microelectrode and optical techniques on several types of preparation (sheep myocardium, sheep Purkinje cells, mouse myocardium). The morphology of the action potential was identical by both methods; the beginning of phase 0 in particular was identical with both methods, eliminating any mechanical activity. Contraction appeared later, during the plateau phase of the action potential with a measurable interval corresponding to the excitation- contraction coupling time. Remote recordings of action potentials without physical contact with the preparation, should enable very accurate myocardium activation mapping using CCD video techniques.

Action Potentials↗
PubMed1984

A low-cost microcomputer system for automated analysis of intracellular cardiac action potentials.

A microcomputer system for automated analysis of action potentials recorded from cardiac Purkinje fibers is described. The system is based upon a DMD 800 microcomputer built around a Z80 microprocessor. Two different sampling intervals are used for analog-to-digital conversion of action potential recorded from driven fibers. The following parameters can be obtained on-line: action potential amplitude; overshoot; maximum diastolic potential; action potential duration measured both at -60 mV and at 90% of complete repolarization; and maximum rate of rise of the upstroke. The digitized form of five consecutive action potentials can be stored on a floppy disk. The automated system eliminates hand measurements; the on-line analysis of the action potentials during pharmacological interventions allows a rapid appreciation of drug effects.

Action Potentials↗
PubMed1996

Simulation of action potentials from metabolically impaired cardiac myocytes. Role of ATP-sensitive K+ current.

The role of the ATP-sensitive K+ current (IK-ATP) and its contribution to electrophysiological changes that occur during metabolic impairment in cardiac ventricular myocytes is still being discussed. The aim of this work was to quantitatively study this issue by using computer modeling. A model of IK-ATP is formulated and incorporated into the Luo-Rudy ionic model of the ventricular action potential. Action potentials under different degrees of activation of IK-ATP are simulated. Our results show that in normal ionic concentrations, only approximately 0.6% of the KATP channels, when open, should account for a 50% reduction in action potential duration. However, increased levels of intracellular Mg2+ counteract this shortening. Under conditions of high [K+]0, such as those found in early ischemia, the activation of only approximately 0.4% of the KATP channels could account for a 50% reduction in action potential duration. Thus, our results suggest that opening of IK-ATP channels should play a significant role in action potential shortening during hypoxic/ischemic episodes, with the fraction of open channels involved being very low ( < 1%). However, the results of the model suggest that activation of IK-ATP alone does not quantitatively account for the observed K+ efflux in metabolically impaired cardiac myocytes. Mechanisms other than KATP channel activation should be responsible for a significant part of the K+ efflux measured in hypoxic/ischemic situations.

Action Potentials↗
PubMed1976

Membrane potential dependent binding of scorpion toxin to action potential Na+ ionophore.

Depolarization of neuroblastoma cells causes a 70-fold increase in the apparent dissociation constant KD for scorpion toxin enhancement of activation of the action potential Na+ ionophore by veratridine and a large increase in the rate of reversal of scorpion toxin action. Depolarization also inhibits binding of 125I-labeled scorpion toxin to a small number of saturable binding sites on electrically excitable neuroblastoma cells and increases the rate of dissociation of scorpion toxin from these sites. The results suggest that scorpion toxin binds to a regulatory component of the action potential Na+ ionophore whose conformation changes on depolarization.

Action Potentials↗
PubMed1998

Control of L-type calcium current during the action potential of guinea-pig ventricular myocytes.

1. During an action potential the L-type Ca2+ current (ICa,L) activates rapidly, then partially declines leading to a sustained inward current during the plateau phase. The reason for the sustained part of ICa,L has been investigated here. 2. In the present study the mechanisms controlling the ICa,L during an action potential were investigated quantitatively in isolated guinea-pig ventricular myocytes by whole-cell patch clamp. To measure the actual time courses of ICa,L and the corresponding L-type channel inactivation (fAP) during an action potential, action potential-clamp protocols combined with square pulses were applied. 3. Within the first 10 ms of the action potential the ICa,L rapidly inactivated by about 50 %; during the plateau phase inactivation proceeded to 95 %. Later, during repolarization, the L-type channels recovered up to 25 %. 4. The voltage-dependent component of inactivation during an action potential was determined from measurements of L-type current carried by monovalent cations. This component of inactivation proceeded rather slowly and contributed only a little to fAP. ICa,L during an action potential is thus mainly controlled by Ca2+-dependent inactivation. 5. In order to investigate the source of the Ca2+ controlling fAP, internal Ca2+ homeostasis was manipulated by the use of Ca2+ buffers (EGTA, BAPTA), by blocking Na+-Ca2+ exchange, or by blocking Ca2+ release from the sarcoplasmic reticulum (SR). Internal BAPTA markedly reduced the L-type channel inactivation during the entire action potential, whereas EGTA affected fAP only during the middle and late plateau phases. Inhibition of Na+-Ca2+ exchange markedly increased inactivation of L-type channels. Although blocking SR Ca2+ release decreased the fura-2-measured cytoplasmic Ca2+ concentration ([Ca2+]i) transient by about 90 %, it reduced L-type channel inactivation only during the initial 50 ms of the action potential. Thus, it is Ca2+ entering the cell through the L-type channels that controls the inactivation process for the majority of the action potential. Nevertheless, SR Ca2+-release contributes 40-50 % to L-type channel inactivation during the initial period of the action potential. However, the maximum extent of inactivation reached during the plateau is independent of Ca2+ released from the SR. 6. For the first time, the actual time course of L-type channel inactivation has been directly determined during an action potential under various defined [Ca2+]i conditions. Thereby, the relative contribution to ICa,L inactivation of voltage, Ca2+ entering through L-type channels, and Ca2+ being released from the SR could be directly demonstrated.

Action Potentials↗
PubMed1994

Adenosine decreases action potential duration by modulation of A-current in rat locus coeruleus neurons.

The possibility that adenosine modulates voltage-dependent conductances in locus coeruleus neurons was investigated in current-clamp and voltage-clamp experiments in a totally submerged rat brain slice preparation. Adenosine (100 microM) reduced the duration of control action potentials and action potentials prolonged by 1 mM barium. Adenosine (100 microM) also reduced the amplitude and slightly reduced the duration of TTX-resistant "calcium" action potentials. Action potential duration was also reduced by the adenosine receptor agonist 2-chloroadenosine in a concentration-dependent manner and the adenosine-induced reduction of action potential duration was blocked by the adenosine receptor antagonist 8-(p-sulfophenyl)theophylline, indicating that this action of adenosine is mediated by an adenosine receptor. The adenosine-induced reduction of action potential duration persisted in the presence of externally applied tetraethylammonium ion (6 mM) and cesium (3 mM). By contrast, adenosine did not reduce the duration of the action potential in the presence of 500 microM 4-aminopyridine (4-AP). Furthermore, 4-AP (30 microM) blocked the adenosine-induced reduction of action potential duration recorded in the presence of 1 mM barium. These data suggested that adenosine may be acting on the voltage-dependent, 4-AP-sensitive potassium current, IA. Single-electrode voltage clamp was used to study IA directly. IA was activated by depolarizing voltage pulses from a hyperpolarized holding potential and was blocked by 1 mM 4-AP. Adenosine (300 microM) enhanced IA by shifting the steady-state inactivation curve in the depolarizing direction.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1990

Correlation of monosynaptic field potentials evoked by single action potentials in single primary afferent axons and their bouton distributions in the dorsal horn.

The relationship between structure and function of the projections of single identified primary cutaneous axons was investigated by recording cord dorsum potentials at 4 sites in response to electrical stimulation of the single axon and visualizing the boutons of the axon stained by intracellular injection of horseradish peroxidase. The rostrocaudal extent of boutons differed from fiber to fiber ranging from 4.14-11.50 mm; their location in the dorsal horn also varied in agreement with the known somatotopy of the presynaptic neuropil and dorsal horn neurons. Rostrocaudal distributions of cord dorsum potentials and boutons of individual fibers revealed good agreement. Cord dorsum potential amplitude and length of the spinal projection were positively correlated with number of boutons, but no correlation with bouton density was found. The spinal projection of afferents innervating slowly adapting type 1 mechanoreceptors exhibited a greater rostrocaudal extent (mean: 8.48 mm) than those innervating rapidly adapting mechanoreceptors (i.e., hair follicle and field receptors: mean: 5.87 mm). Although the mean total number of boutons was greater for axons with slowly adapting receptors (7,250/fiber) than for axons of rapidly adapting receptors (4,677/fiber), no differences in the longitudinal density of boutons (boutons/mm) were observed. Likewise, summed amplitudes of cord dorsum potentials at the 4 recording electrodes were larger for SA1 afferents than for those of field and hair follicle afferents. A major role for the number of boutons in determining these differences is supported by the finding that the calculated average contribution per bouton to cord dorsum potentials (expressed as an amplitude coefficient a) was similar for slowly and rapidly adapting afferents. No evidence was found for regions in which boutons did not contribute to the cord dorsum potential.

Action Potentials↗
PubMed1989

Changes in cytosolic calcium monitored by inward currents during action potentials in guinea-pig ventricular cells.

Action potentials were recorded from single cells isolated from guinea-pig ventricular muscle. Contraction was measured with an optical technique. Tail currents thought to be activated by cytosolic calcium were recorded when action potentials were interrupted by application of a voltage-clamp. A family of tail currents was recorded by interrupting the action potential at various times after the upstroke. The envelope of tail current amplitudes was taken as an index of changes in cytosolic calcium. Consistent with this interpretation, tail currents were negligible following intracellular loading with the calcium chelator BAPTA to suppress calcium transients. The cytosolic calcium transient estimated from the envelope of tails reached a peak approximately 50 ms after the upstroke of the action potential, and fell close to diastolic levels before repolarization was complete; 10 mM caffeine delayed the time to peak contraction, and caused a prolongation of the cytosolic calcium transient estimated from the envelope of tail currents. Caffeine also induced the appearance of a distinct late plateau phase of the action potential. Intracellular BAPTA suppressed the late plateau, contraction and tail currents in cells exposed to caffeine. Exposure to caffeine increased the time constant for decay of tail currents (from approximately 25 to 70 ms). When action potentials were greatly abbreviated by interruption with a voltage-clamp, a progressive decline occurred in the subsequent three contractions and tail currents. There was a progressive reversal of these effects over four responses when the full action potential duration was restored. None of these effects was observed in cells exposed to caffeine. Calcium-activated tail currents appear to be a useful qualitative index of changes in cytosolic calcium. The observations are consistent with the suggestion that cytosolic calcium is reduced during the plateau by a combination of calcium extrusion through Na-Ca exchange and calcium uptake into caffeine-sensitive stores. It also appears that reduction of stores loading during abbreviated action potentials reduces subsequent contraction in cells not exposed to caffeine.

Action Potentials↗
PubMed1983

Action potential in neurons of motor nerve net of Cyanea (Coelenterata).

Neurons of the motor nerve net of the jellyfish Cyanea were impaled with microelectrodes for intracellular recordings. The cells have conventional, negative resting potentials and produce variable-amplitude action potentials with complex waveforms. The variability and complexity of these spikes is due to the superimposition of two classes of Ca2+-dependent potentials on an otherwise fast, clean action potential. Repetitive stimulation and ionic manipulation reveal that most superimposed potentials are chemically induced excitatory postsynaptic potentials (EPSPs). These account for the complexity and variability of the action potential. The remaining potential is interpreted as a Ca2+ component of the action potential. The action potential is a Na+-dependent but tetrodotoxin- (TTX) insensitive event. Repolarization is achieved by two pharmacologically distinct mechanisms: a tetraethylammonium- (TEA) and 4-amino-pyridine- (4-AP) sensitive K+ efflux and a delayed, Ca2+-activated, K+ efflux. The latter is responsible for the afterhyperpolarization that follows the action potential. The results indicated that these neurons are physiologically conventional. This is interesting in view of the phylogenetic primitiveness of the preparation and important, since it means that this preparation can provide generally useful information on chemical synaptic physiology.

4-Aminopyridine↗
PubMed1989

Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts.

Stretch of excised myocardial tissue causes electrophysiological and potentially arrhythmogenic changes in transmembrane action potentials but corresponding data of the intact mammalian heart are lacking. The effects of increases in ventricular volume and pressure on epicardial monophasic action potentials were therefore investigated in isolated, cross circulated and in situ canine hearts. In seven isolated hearts, increases in ventricular volume and pressure resulted in (1) a linearly related decrease in action potential amplitude (r = 0.988; slope = 0.41% amplitude.ml-1; volume intercept = 17.6 ml), mainly due to a decrease in maximum diastolic potential; (2) a decrease in action potential plateau duration (at 20% repolarisation) by 19 (SD 8)%; and (3) appearance of early afterdepolarizations, reaching up to 18% of total action potential amplitude. Afterdepolarizations occurred only when ventricular outflow was obstructed at end diastole but not at end systole. In eight in situ hearts, increase in left intraventricular pressure produced by transient occlusions of the ascending aorta was also accompanied by decrease in maximum diastolic potential and action potential plateau duration, and by appearance of early afterdepolarizations. In both isolated and in situ intact ventricles, the loading induced electrophysiological changes were associated with occurrence of ectopic ventricular beats. These data show that mechanical overload produces significant electrophysiological changes in the intact canine ventricle which may lead to arrhythmia.

Action Potentials↗
PubMed1986

Activity-dependent depression of nerve action potential by phenytoin.

The action of the anticonvulsant drug phenytoin was investigated on the responsiveness of isolated amphibian and human nerves to repetitive stimulation. At low frequencies of stimulation (0.5-25 Hz) the drug (at a concentration of 0.1 mM) had no notable effect on the compound nerve action potential. By contrast, at higher rates of stimulation (50-300 Hz), it produced a progressive decrease in amplitude and integral of the compound action potential. This effect was positively correlated with the frequency of nerve activation and was markedly enhanced by elevating the extracellular K+ concentration. Thus, phenytoin induces a use- and frequency-dependent depression of axon conduction, which may contribute to its preferential suppression of the spread of high-frequency seizure discharge in the brain.

Action Potentials↗