SEARCH · PubMed Health

Results for “Action Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

PubMed1983

Computer analysis of prolongation of cardiac action potential duration.

Using Beeler and Reuter's mathematical model of action potential in myocardial fibers, a similar extent of prolongation of action potential duration at -60 mV (APD -60) was produced at the infinite interval of stimulation by altering parameter values for slow inward current (is) time-independent (ik1) and time-dependent (ix1) outward currents. Among five types of prolongation of APD -60 thus produced, the plateau height is high in two types at this interval, but in three at a shorter interval. The degree of prolongation varies between these five types at this shorter interval. The stimulus interval-action potential duration (interval-duration) relation curves reflect changes in time-dependent parameters of these currents. Thus various types of APD prolongation may be distinguished from each other by the different behavior of action potentials at low and high frequencies of stimulation. ix1 increases by 40-fold at the moment of the maximum rate of depolarization at an interval of 330 msec, but is still negligibly small as compared with sodium current.

Action Potentials↗

PubMed2001

Action potential threshold of hippocampal pyramidal cells in vivo is increased by recent spiking activity.

Understanding the mechanisms that influence the initiation of action potentials in single neurons is an important step in determining the way information is processed by neural networks. Therefore, we have investigated the properties of action potential thresholds for hippocampal neurons using in vivo intracellular recording methods in Sprague-Dawley rats. The use of in vivo recording has the advantage of the presence of naturally occurring spatio-temporal patterns of synaptic activity which lead to action potential initiation. We have found there is a large variability in the threshold voltage (5.7+/-1.7 mV; n=22) of individual action potentials. We have identified two separate factors that contribute to this variation in threshold: (1) fast rates of membrane potential change prior to the action potential are associated with more hyperpolarized thresholds (increased excitability) and (2) the occurrence of other action potentials in the 1 s prior to any given action potential is associated with more depolarized thresholds (decreased excitability). We suggest that prior action potentials cause sodium channel inactivation that recovers with approximately a 1-s time constant and thus depresses action potential threshold during this period.

Action Potentials↗

PubMed1976

Divalent cations and the action potential of leech Retzius cells.

The effects of Sr, Ba, Mn, La and Co on the action potential of the leech Retzius cell were examined using intracellular recording techniques. A previous paper showed that these cells could fire Ca-dependent action potentials in Na-free solution provided TEA was present (Kleinhaus and Prichard, 1975). Under the same conditions Sr 1.5--20 mM was capable of substituting as a current carrier. Ba 2--25mM added to normal Ringer prolonged the duration and increased the amplitude of the action potential of the Retzius cell, and supported action potentials without requiring TEA in Na-free solutions. The overshoots of the Sr- and Ba-dependent action potentials varied with a slope of 40 mM and 75 mV, respectively per 10-fold change in divalent cation concentration. Mn and La selectively blocked that portion of the action potential resulting from an inward movement of Ca, Sr or Ba without affecting the Na-dependent depolarization. The actions of Ca 1 mM on Sr-dependent action potentials were compatible with reversible competitive antagonism. In conclusion the findings: 1. support the proposition that outward K current must be blocked in order for divalent cations to dominate the Retzius cell's behavior during excitation. 2. characterize the divalent cation conductance channel as pharmacologically distinct from the Na conductance channel in the Retzius cell and similar to those described in several other excitable membranes. 3. suggest that the current carrying divalent cations probably flow through the same channel.

Action Potentials↗

PubMed1997

Reduction in external K causes increased action potential shortening in ventricular myocytes from the spontaneously hypertensive rat.

OBJECTIVES: (1) To study the effect of low external K and combined low K plus low Mg on the action potential of hypertrophied left ventricular myocytes isolated from the spontaneously hypertensive rat (SHR) and cells from normotensive control rats (NCR). (2) To identify differences in the response of SHR and NCR ventricular myocytes to low K and low K plus low Mg that could contribute to the increased number of arrhythmias observed in hypertrophied hearts. METHODS: Cells were superfused with Tyrode's solution containing 6 mmol/l K and stimulated at 1 Hz. Action potentials were recorded using the patch clamp technique. The effect of low K (2.4 mmol/l) and combined low K plus low Mg (2.4 mmol/l K and nominally zero Mg) on the characteristics of the action potential was measured in nine SHR, eight Wistar-Kyoto rat and 5 Wistar rat cells. RESULTS: With 6 mmol/l K, the action potential was prolonged significantly in SHR cells at 50, 70, 90 and 95% repolarizations. Both low K and low K plus low Mg shortened the action potential significantly only at 70% repolarization in NCR cells. In contrast, both low K and low K plus Mg led to marked action potential shortening at 70 and 90% repolarizations in SHR cells (P < 0.01) and also at 50 and 95% repolarizations (P < 0.05). Combined low K plus low Mg produced no additional effect on the action potential shape either in SHR or in NCR cells compared with that produced by low K alone. Although in SHR cells low K and combined low K plus low Mg produced a greater shortening of the action potential, which extended across a longer period of repolarization, a significant prolongation of the action potential still remained with low K at 50 and 95% repolarizations in SHR cells compared with that in NCR cells. CONCLUSIONS: Low K shortened the action potential both in NCR and in SHR cells but had a much greater effect on the action potential shape in SHR cells. Low K attenuated the difference in action potential shape between SHR and NCR by reducing the longer plateau observed in SHR cells. Combined low K plus low Mg exerted an effect on the action potential shape similar to that of low K alone in all cells. This increased shortening of the action potential produced by low K in SHR cells might be relevant to the increased incidence of arrhythmias associated with left ventricular hypertrophy, perhaps by shortening the wavelength of excitation and encouraging re-entrant arrhythmias, or by increasing the heterogeneity of repolarization within the ventricle.

Action Potentials↗

PubMed1990

Computation of action potential propagation and presynaptic bouton activation in terminal arborizations of different geometries.

Action potential propagation in axons with bifurcations involving short collaterals with synaptic boutons has been simulated using SPICE, a general purpose electrical circuit simulation program. The large electrical load of the boutons may lead to propagation failure at otherwise uncritical geometric ratios. Because the action potential gradually fails while approaching the branch point, the electrotonic spread of the failing action potential cannot depolarize the terminal boutons above an assumed threshold of 20 mV (Vrest = 0 mV) for the presynaptic calcium inflow, and therefore fails to evoke transmitter release even for boutons attached at short collaterals. For even shorter collaterals the terminal boutons can again be activated by the spread of passive current reflected at the sealed end of the bouton which increases the membrane potential above firing threshold. The action potential is then propagated in anterograde fashion into the main axon and may activate the terminal bouton on the other collateral. Differential activation of the synaptic boutons can be observed without repetitive activation of the main axon and with the assumption of uniform membrane properties. Axon enlargements above a critical size at branch points can increase the safety factor for propagation significantly and may serve a double function: they can act both as presynaptic boutons and as boosters, facilitating invasion of the action potential into the terminal arborizations. The architecture of the terminal arborizations has a profound effect on the activation pattern of synapses, suggesting that terminal arborizations not only distribute neural information to postsynaptic cells but may also be able to process neural information presynaptically.

Action Potentials↗

PubMed1994

The biphasic morphology of voluntary and spontaneous single muscle fiber action potentials.

The extracellular morphology of single muscle fiber action potentials (SMFAPs) is anticipated by volume conductor theory to be triphasic. Single muscle fiber action potentials recorded during single muscle fiber studies (500 Hz to 20 kHz) usually appear triphasic; however, when recorded with an open bandwidth (1 Hz to 20 kHz) they are found to be biphasic. Fibrillation potentials recorded with a single fiber electrode and open bandwidth have identical biphasic morphologies as volitional SMFAPs. Computer simulations suggest that the intracellular action potential models currently used to derive simulated extracellularly recorded SMFAPs must have the repolarization phase considerably prolonged to yield the clinically recorded potentials. This implies that either the models presently used require significant modification, or there is some distortion of the transmembrane source current induced in needle recording studies such that biphasic and not triphasic potentials are detected.

Action Potentials↗

PubMed2003

D-amphetamine-elicited action potential bursts in central snail neurons: role of second messenger systems.

BACKGROUND AND PURPOSE: Neuronal bursts of action potentials are closely related to seizure activity. Amphetamine rarely induces seizures at therapeutic doses, but seizure may occur after the first dose. This study investigated factors affecting d-amphetamine-elicited action potential bursts in isolated central snail neurons. METHODS: The central right parietal neuron 1 (RP1 neuron) from the subesophageal ganglia of the African snail Achatina fulica Ferussac was used to evaluate neurotransmitter systems involved in d-amphetamine-elicited potential burst activity by use of conventional electrophysiological and general pharmacological techniques. RESULTS: d-Amphetamine (135 and 270 microM) elicited bursts of action potentials in the RP1 neuron in a concentration dependent manner. The burst activity was not blocked by pretreatment with prazosin (100 microM), yohimbine (100 microM), propranolol (100 microM), atropine (1 mM), or by continuous perfusion of calcium-free solution. These results suggest that the burst activity elicited by d-amphetamine was not due to activation of the cholinergic or adrenergic receptors of the excitable membrane. The burst firing of action potentials was decreased following extracellular application of the specific protein kinase A inhibitors H89 (N-[2-(p-bromocinnamylamino)-ethyl]-5-isoquinoline sulfonamide, 10 microM), or KT-5720 (10 microM). However, the burst firing of action potentials was not affected after extracellular application of the specific protein kinase C inhibitors Ro 31-8220 (10 microM) or chelerythrine (10 microM). Forskolin (10 microM), an activator of adenylyl cyclase, facilitated the burst firing of action potentials elicited by d-amphetamine. However, in the absence of d-amphetamine, a higher concentration of forskolin (100 microM) was able to elicit burst firing of action potentials. CONCLUSIONS: These results suggest that the action potential bursts elicited by d-amphetamine are associated with the cyclic adenosine monophosphate (cAMP) second messenger system and are not related to the cholinergic or adrenergic receptors or protein kinase C activity in the RP1 snail neuron.

Action Potentials↗

PubMed2006

Voltage noise influences action potential duration in cardiac myocytes.

Stochastic gating of ion channels introduces noise to membrane currents in cardiac muscle cells (myocytes). Since membrane currents drive membrane potential, noise thereby influences action potential duration (APD) in myocytes. To assess the influence of noise on APD, membrane potential is in this study formulated as a stochastic process known as a diffusion process, which describes both the current-voltage relationship and voltage noise. In this framework, the response of APD voltage noise and the dependence of response on the shape of the current-voltage relationship can be characterized analytically. We find that in response to an increase in noise level, action potential in a canine ventricular myocytes is typically prolonged and that distribution of APDs becomes more skewed towards long APDs, which may lead to an increased frequency of early after-depolarization formation. This is a novel mechanism by which voltage noise may influence APD. The results are in good agreement with those obtained from more biophysically-detailed mathematical models, and increased voltage noise (due to gating noise) may partially underlie an increased incidence of early after-depolarizations in heart failure.

Action Potentials↗

PubMed1997

The effect of alterations to action potential duration on beta-adrenoceptor-mediated aftercontractions in human and guinea-pig ventricular myocytes.

Aftercontractions induced by beta-adrenoceptor stimulation in human and guinea-pig cardiomyocytes may be related to changes in action potential duration (APD). We investigated the effects of altering APD during the occurrence of isoproterenol-induced aftercontractions, using the KATP channel openers cromakalim and lemakalim or the action potential voltage clamp technique, in guinea-pig and human ventricular cardiomyocytes. Contractile responses were measured at 32 degrees C using a video-based edge-detection system. In guinea-pig myocytes, action potentials, Indo-1 fluorescence and contraction were measured at 22 degrees C. Isoproterenol (< or = 12 nM) had variable effects on APD but induced aftercontractions, the majority (14/19 cells) of which occurred during the action potential. Short action potentials were produced using K+ channel openers. These compounds reduced or completely abolished the isoproterenol-induced aftercontractions. Increasing isoproterenol in the presence of K+ channel opener restored the main contraction to a level similar to or above those with isoproterenol alone, but without the reappearance of aftercontractions. When cells were stimulated to contract under action potential voltage clamp, isoproterenol-induced aftercontractions were abolished by voltage clamping with action potentials of short duration. It was possible to induce aftercontractions in some cells without application of isoproterenol if voltage clamp-imposed action potentials of very long duration were used. These aftercontractions were also abolished by shortening action potential duration. We conclude that K+ channel openers or the imposition of action potentials of short duration can dissociate positively inotropic beta-adrenoceptor stimulation from aftercontraction formation and that action potentials of long duration can be pro-arrhythmic.

Action Potentials↗

PubMed2003

[Effect of deoxynivalenol on action potentials of cultured cardiomyocytes and the protective effects of selenium].

OBJECTIVE: To study the effect of deoxynivalenol (DON), a mycotoxin produced by Fusarium graminearum, on action potentials of cultured cardiomyocytes and the possible protective effects of sodium selenite. METHODS: Ventricular myocytes from neonatal Wistar rats were cultured, and the transmembrane action potentials were recorded with glass microelectrodes before and after addition of DON at different concentrations. The cultured cardiomyocytes were pretreated with 0.5 mg/L selenium (as sodium selenite) to observe the protective effects of selenium against the effects of DON. RESULTS: DON at concentrations of 50, 100 and 200 mg/L decreased the action potential parameters including action potential amplitude (APA), overshoot (OS), threshold potential (TP), maximum rate of depolarization (Vmax) and action potential discharging frequency (APF), and prolonged the action potential duration of 10%, 50% and 90% repolarization (APD(10), APD(50) and APD(90)). Some of the parameters, such as APA, Vmax, APD and APF, changed in a concentration-dependent manner. The cultured cardiomyocytes pretreated with 0.5 mg/L of selenium for about 16 h presented only slight changes in action potential parameters induced by 200 mg/L DON. CONCLUSIONS: DON inhibit the membrane action potentials of cardiomyocytes, suggesting DON may interfere with the transmembrane movement of Ca(2+) and K(+), and sodium selenite may decrease the toxic effect of DON on cultured cardiomyocytes.

Action Potentials↗

PubMed1982

Further studies of rapid mechanical changes in squid giant axon associated with action potential production.

Mechanical changes in the squid giant axon associated with the production of an action potential are examined further by using piezoelectric and optical methods. The peak of swelling of the axon coincides with the peak of the action potential recorded internally at the site of mechanical recording. Mechanical changes produced by a train of action potentials do not summate. Repetitively fired action potentials induced by lowering the external Ca-ion concentration are preceded by a gradual swelling of the axon. An inward current through the membrane causes shrinkage and an outward current produced swelling of the axon. An inward current enhances and an outward current depresses the mechanical changes associated with the action potential. There is a transient shortening followed by an elongation of the axon when an action potential travels along the axon. It is argued that the experimental results obtained are consistent with the colloid chemical, or macromolecular, theory of excitation.

Action Potentials↗

PubMed2005

Backpropagating action potentials in neurones: measurement, mechanisms and potential functions.

Here we review some properties and functions of backpropagating action potentials in the dendrites of mammalian CNS neurones. We focus on three main aspects: firstly the current techniques available for measuring backpropagating action potentials, secondly the morphological parameters and voltage gated ion channels that determine action potential backpropagation and thirdly the potential functions of backpropagating action potentials in real neuronal networks.

Action Potentials↗

PubMed1999

Mechanisms and consequences of action potential burst firing in rat neocortical pyramidal neurons.

1. Electrophysiological recordings and pharmacological manipulations were used to investigate the mechanisms underlying the generation of action potential burst firing and its postsynaptic consequences in visually identified rat layer 5 pyramidal neurons in vitro. 2. Based upon repetitive firing properties and subthreshold membrane characteristics, layer 5 pyramidal neurons were separated into three classes: regular firing and weak and strong intrinsically burst firing. 3. High frequency (330 +/- 10 Hz) action potential burst firing was abolished or greatly weakened by the removal of Ca2+ (n = 5) from, or by the addition of the Ca2+ channel antagonist Ni2+ (250-500 microm; n = 8) to, the perfusion medium. 4. The blockade of apical dendritic sodium channels by the local dendritic application of TTX (100 nM; n = 5) abolished or greatly weakened action potential burst firing, as did the local apical dendritic application of Ni2+ (1 mM; n = 5). 5. Apical dendritic depolarisation resulted in low frequency (157 +/- 26 Hz; n = 6) action potential burst firing in regular firing neurons, as classified by somatic current injection. The intensity of action potential burst discharges in intrinsically burst firing neurons was facilitated by dendritic depolarisation (n = 11). 6. Action potential amplitude decreased throughout a burst when recorded somatically, suggesting that later action potentials may fail to propagate axonally. Axonal recordings demonstrated that each action potential in a burst is axonally initiated and that no decrement in action potential amplitude is apparent in the axon > 30 microm from the soma. 7. Paired recordings (n = 16) from synaptically coupled neurons indicated that each action potential in a burst could cause transmitter release. EPSPs or EPSCs evoked by a presynaptic burst of action potentials showed use-dependent synaptic depression. 8. A postsynaptic, TTX-sensitive voltage-dependent amplification process ensured that later EPSPs in a burst were amplified when generated from membrane potentials positive to -60 mV, providing a postsynaptic mechanism that counteracts use-dependent depression at synapses between layer 5 pyramidal neurons.

Action Potentials↗

PubMed1989

[Effects of bis(dimethyl amino)-diphenyl methane (BDDM) on action potentials in guinea pig papillary muscle].

The effects of BDDM on action potentials and slow response action potentials in guinea pig papillary muscle were investigated by microelectrode technique. BDDM prolonged action potentials duration at 30, 50, 90, and 100% repolarization (APD30, APD50, APD90, APD100) and prolonged the effective refractory period (ERP), so ERP/APD value became greater. BDDM (51.6 mumol/L) decreased the APA, Vmax and prolonged APD50, APD90. In barium-induced ventricular autorhythmicity, BDDM suppressed the maximal diastolic potential (MDP), APA and reduced the rate of spontaneous rhythm. The results suggest that BDDM may unspecifically inhibit the currents of Ca2+, K+, and Na+.

Action Potentials↗

PubMed1988

Dependence between intra- and extracellular action potentials of isolated frog muscle fibres at different temperatures.

The intra- and extracellular action potentials of isolated frog muscle fibre immersed in a volume conductor at different temperatures are described. It was found that upon increasing the temperature the amplitude of the first time derivative of the intracellular action potentials increased linearly, whereas the amplitude of the second time derivative increased nonlinearly. The duration of the separate phases of the time derivatives shortened upon heating, as the velocity of spreading of the excitation increased. The length of the separate phases of the space derivatives of the action potential shortened when increasing the temperature. The amplitudes of the space derivatives were calculated. The changes in the derivatives of the action potential were explained by the influence of the temperature on the peak inward and outward transmembrane current. The changes in the extracellular action potentials produced by the temperature near the membrane and at longer radial distance at points far and near the end of the fibre are described. They were explained by the changes in the space derivatives of the intracellular action potential as well as by the features of the distribution of the extracellular potential field in the volume conductor around the finite-in-length excitable fibre.

Action Potentials↗

PubMed2006

Mechanism for action potential alternans: the interplay between L-type calcium current and transient outward current.

BACKGROUND: The ionic mechanisms underlying action potential duration alternans are not established. OBJECTIVES: The purpose of this study was to explore the mechanisms underlying action potential alternans. METHODS: Computer simulations were performed using a model of a single ischemic myocyte. To emulate ischemia, extracellular potassium was raised to 10 mM, L-type calcium channel conductance was decreased, and the conductivity of the transient outward current I(to)was varied. RESULTS: Alternans occurred at basic cycle lengths between 350 and 1,800 ms. The alternans resulted from the interplay of the recovery kinetics of the calcium and transient outward current inactivation gates. Depending on the diastolic interval, the transient outward current was sufficiently strong and calcium current sufficiently weak to result in the abolition of the action potential plateau and thus in an abbreviated action potential. The inactivation and recovery kinetics of the inactivation gates were such that calcium current was relatively stronger than transient outward current after an abbreviated action potential. The subsequent action potential was long because calcium current was sufficiently large to restore the action potential plateau dome after the partial repolarization caused by the transient outward current. The long-short pattern repeated indefinitely. This alternans mechanism explains how 2:1 patterns can evolve into 3:1 patterns, as observed in at least one experiment, as ischemia progresses and calcium current diminishes. CONCLUSION: Computer simulations and basic theory suggest that the interplay between L-type calcium and transient outward currents causes at least one type of alternans.

Action Potentials↗

PubMed2001

Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons.

C-type dorsal root ganglion (DRG) neurons can generate tetrodotoxin-resistant (TTX-R) sodium-dependent action potentials. However, multiple sodium channels are expressed in these neurons, and the molecular identity of the TTX-R sodium channels that contribute to action potential production in these neurons has not been established. In this study, we used current-clamp recordings to compare action potential electrogenesis in Na(v)1.8 (+/+) and (-/-) small DRG neurons maintained for 2-8 h in vitro to examine the role of sodium channel Na(v)1.8 (alpha-SNS) in action potential electrogenesis. Although there was no significant difference in resting membrane potential, input resistance, current threshold, or voltage threshold in Na(v)1.8 (+/+) and (-/-) DRG neurons, there were significant differences in action potential electrogenesis. Most Na(v)1.8 (+/+) neurons generate all-or-none action potentials, whereas most of Na(v)1.8 (-/-) neurons produce smaller graded responses. The peak of the response was significantly reduced in Na(v)1.8 (-/-) neurons [31.5 +/- 2.2 (SE) mV] compared with Na(v)1.8 (+/+) neurons (55.0 +/- 4.3 mV). The maximum rise slope was 84.7 +/- 11.2 mV/ms in Na(v)1.8 (+/+) neurons, significantly faster than in Na(v)1.8 (-/-) neurons where it was 47.2 +/- 1.3 mV/ms. Calculations based on the action potential overshoot in Na(v)1.8 (+/+) and (-/-) neurons, following blockade of Ca(2+) currents, indicate that Na(v)1.8 contributes a substantial fraction (80-90%) of the inward membrane current that flows during the rising phase of the action potential. We found that fast TTX-sensitive Na(+) channels can produce all-or-none action potentials in some Na(v)1.8 (-/-) neurons but, presumably as a result of steady-state inactivation of these channels, electrogenesis in Na(v)1.8 (-/-) neurons is more sensitive to membrane depolarization than in Na(v)1.8 (+/+) neurons, and, in the absence of Na(v)1.8, is attenuated with even modest depolarization. These observations indicate that Na(v)1.8 contributes substantially to action potential electrogenesis in C-type DRG neurons.

Action Potentials↗

PubMed1977

Developmental changes in the inward current of the action potential of Rohon-Beard neurones.

1. Rohon-Beard cells in the spinal cord of Xenopus tadpoles have been studied in animals from early neural tube to free-swimming larval stages. The onset and further development of electrical excitability of these neurones has been investigated in different ionic environments, to determine the ionic species carrying the inward current of the action potential.2. The cells appear inexcitable at early stages (Nieuwkoop & Faber stages 18-20) and do not give action potentials to depolarizing current pulses.3. The action potential is first recorded at stage 20. (A) The inward current is carried by Ca(2+) at stages 20-25, since it is blocked by mm quantitites of La(3+), Co(2+) or Mn(2+) and is unaffected by removal of Na(+) or the addition of tetrodotoxin (TTX). (B) The action potential is an elevated plateau of long duration (mean 190 msec at stages 20-22). The duration decreases exponentially with repetitive stimulation. (C) The specific Ca(2+) conductance (g(Ca)) at the onset of the plateau of the action potential is 2.6 x 10(-4) mho/cm(2). Calculations show that a single action potential raises [Ca(2+)](1) by more than 100-fold.4. At later times (stages 25-40), the inward current of the action potential is carried by both Na(+) and Ca(2+): the action potential has two components, an initial spike which is blocked by removal of Na(+) or addition of TTX, followed by a plateau which is blocked by La(3+), Co(2+) or Mn(2+).5. Finally (stages 40-51), the inward current is primarily carried by Na(+), since the action potential is blocked only by removal of Na(+) or addition of TTX, and the overshoot agrees with the prediction of the Nernst equation for a Na-selective membrane. When the outward current channel is blocked and cells exposed to Na-free solutions, 67% of cells at the latest stages studied were incapable of producing action potentials in which the inward current is carried by divalent cations.6. The duration of the action potential decreases from a maximum of about 1000 msec to about 1 msec during development. The maximum input resistance (R(in)) decreases from ca. 1000 to 100 MOmega.7. The calcium action potential may play a role in the development of excitability and the growth of the neurones.

Action Potentials↗