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PubMed1985

Ventricular action potentials, ventricular extracellular potentials, and the ECG of guinea pig.

Action potentials were recorded from different regions of the guinea pig ventricle to characterize regional differences in waveform configuration, and to acquire insight into the generation of the T-wave of the electrocardiogram. Isolated tissue preparations were driven at 1 Hz, and microelectrodes were used to map accessible surface regions of the epicardium, endocardium, and septum. There were minimal differences in regional resting potentials (mean -87 mV) and amplitudes (mean 122 mV), but Vmax in the epicardium (mean 110 V/sec) was much smaller than elsewhere (mean 247 V/sec). The action potential duration at the -80 mV repolarization level was longest in the papillary muscles (mean 154 msec), shortest in the septum (mean 126 msec), and generally 10-15 msec longer at the base than at the apex. The characteristics of intramural action potentials were inferred from measurements on enzymatically isolated myocytes, the rationale being that most dissociated myocytes originated from intramural cell layers. The action potentials in about 40% of the myocytes had durations similar to those recorded from the tissue surface (110-170 msec), and the remainder ranged from 170-290 msec long. The existence of longer-than-surface action potentials in the ventricle was also inferred from the body surface electrocardiogram and from bipolar electrograms of isolated left ventricles. In both cases, the Q-T intervals could be accounted for only by action potentials longer than those recorded from the ventricular surface.

Action Potentials↗

PubMed1971

Na and Ca components of action potential in amphioxus muscle cells.

1. The ionic mechanism of the action potential produced in lamella-like muscle cells of amphioxus, Branchiostoma californiense, was investigated with intracellular recording and polarization techniques.2. The resting potential and action potential overshoot in normal saline are -53+/-5 mV (S.D.) and +29+/-10 mV (S.D.) respectively.3. The action potential is eliminated by tetrodotoxin (3 muM) and by replacing NaCl in the saline with Tris-chloride but maintained by replacing Na with Li.4. After elimination of the normal action potential by tetrodotoxin or replacing Na with Tris, the addition of procaine (7.3 mM) to the external saline makes the membrane capable of producing a regenerative potential change.5. The peak potential of the regenerative response depends on external Ca concentration in a manner predicted by the Nernst equation with Ca concentrations close to normal.6. The Ca dependent response is reversibly suppressed by Co or La ions.7. Similar regenerative responses are obtained when Ca is substituted with Sr or Ba.8. It is concluded that two independent mechanisms of ionic permeability increase occur in the membrane of amphioxus muscle cell, one to Na and the other to Ca.

Action Potentials↗

PubMed1990

A new single catheter technique for simultaneous measurement of action potential duration and refractory period in vivo.

In vivo correlations of action potential duration measured by a monophasic action potential catheter and effective refractory period measured by a separate pacing catheter have been poor, probably because of the known variability of both action potential duration and effective refractory period between different ventricular sites. In this study, a new quadripolar contact electrode catheter designed for simultaneous pacing and monophasic action potential recording at closely adjacent sites (2 mm separation between recording electrodes and pacing electrodes) was tested in five closed chest dogs and four patients. Dog studies: Pacing thresholds were extremely low, ranging from 0.02 to 0.25 mA (mean +/- SD 0.099 +/- 0.051, n = 36) and were stable over time (less than 20% increase during 1 h of continuous pacing). Because of the close proximity of pacing and recording electrodes, the pacing artifact nearly coincided with the monophasic action potential upstroke. Because of the low pacing threshold, however, pacing artifacts were small (33 +/- 17% of the monophasic action potential amplitude at twice diastolic threshold strength) and did not affect the duration or configuration of the simultaneously recorded monophasic action potential. The short stimulus response time and the undisturbed monophasic action potential signal fidelity during pacing allowed precise simultaneous measurements of action potential duration and effective refractory period at the same endocardial site.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1999

Determinants of motor unit action potential duration.

OBJECTIVE: Motor unit action potential (MUAP) recordings are modeled by means of a single muscle fiber simulation program, to define two key subcomponents comprising the complete physiologic MUAP duration. A number of defining properties of these subcomponents are further developed. METHODS: A single muscle fiber simulation program is utilized with various muscle fiber lengths and conduction velocities to generate near-field and far-field waveforms. RESULTS: Two key subcomponents to the total physiologic single muscle fiber and hence MUAP duration are identified. One, defined as the near-field component, is directly dependent upon muscle fiber hemi-length. The other, defined as the far-field component, is independent of fiber length, but matches the internal action potential in duration. Both the near-field and far-field components are inversely dependent upon intracellular action potential conduction velocity. Additionally, temporal dispersion among the individual fibers contributing to a MUAP must be included in the overall MUAP duration calculation. CONCLUSIONS: It is hoped that this approach to MUAP duration may allow a more complete appreciation of the components contributing to the MUAP, than permitted by the empirically derived values for MUAP duration presently under clinical use.

Action Potentials↗

PubMedDate not supplied

Effect of argon laser stapedotomy on cochlear potentials. II. Alteration of the compound action potential (CAP).

The influence of the argon laser on inner-ear function during and after laser stapedotomy was investigated in guinea pigs, using the compound action potential (CAP) as parameter. With the onset of the argon laser impact, the CAP is depressed or even extinguished up to 10 s. The temporal course of subsequent CAP recovery is similar to that of endocochlear temperature recovery after laser stapedotomy, so that a direct influence of temperature increase and CAP decrease is probable. No permanent attenuation of CAP amplitude was found after a single laser perforation of the stapes footplate.

Action Potentials↗

PubMedDate not supplied

Effects of histamine H1 receptor antagonists on action potentials in guinea-pig isolated papillary muscles.

The effects of histamine H1 receptor antagonists (H1 antagonists) on action potentials in guinea-pig isolated papillary muscles were examined using a microelectrode technique. Terfenadine (0.03 microM) prolonged the action potential duration at 90% repolarization, without affecting the resting membrane potentials, the action potential amplitude or the maximal upstroke velocity, although its metabolite, terfenadine carboxylate, did not affect any action potential parameters. Astemizole, (+)-chlorpheniramine, and clemastine prolonged the action potential duration at 90% repolarization at 0.03, I and 10 microM, respectively. The action potential duration-prolonging effects of terfenadine and astemizole correspond to the reverse use-dependence phenomenon. However, ebastine and its metabolite, carebastine, did not affect the action potential parameters at 3 microM. Mequitazine, diphenhydramine, epinastine, ketotifen and oxatomide were also without effect at 10 microM. These H1 antagonists suppressed the histamine-induced contractions in guinea-pig isolated ileum longitudinal muscles. However, the potency order was inconsistent with that for prolonging the action potential duration. Terfenadine or astemizole prolonged the action potential duration at concentrations lower than each IC50 value for H1 receptor antagonism. Cimetidine, a H2 receptor antagonist, and thioperamide, a H3 receptor antagonist, had little effect on the action potentials. These results suggest that, in guinea-pig isolated papillary muscles, blockade of histamine receptors does not cause prolongation of the action potential duration, leading to prolongation of electrocardiographic QT intervals, and that H1 antagonists may be classified into three groups: (1) drugs causing prolongation of the action potential duration at concentrations producing H1 antagonism and (2) at concentrations higher than those producing H1 antagonism, and.

Action Potentials↗

PubMed1978

A study of the canine gastric action potential in the presence of tetraethylammonium chloride.

1. The effects of tetraethylammonium (TEA) ion on the action potential of isolated longitudinal muscle of the dog antrum were used to gain some insight into the mechanism of generation of the plateau potential of the action potential complex. The double sucrose gap was used. 2. In concentrations of TEA up to 5 mM, the amplitude of the upstroke potential was increased. In 10mM-TEA there was also an increase in the amplitude of the plateau potential and in the maximum rate of rise of the upstroke potential. 3. Concentrations of TEA (3 mM and greater) increased the duration of the action potential. Five mM-TEA produced spike potentials which occurred only during the plateau potential of the action potential. Each spike caused a contraction. 4. The steady-state voltage-current relation was studied in normal Krebs solution and in TEA containing Krebs solution. In normal Krebs solution the voltage response was not a linear function of the applied current when outward current pulses were used. In TEA solution the voltage response was a linear function of the entire range of applied depolarizing current. 5. In low concentrations of TEA (2-4 mM), when the steady-state voltage-current relation was linear, constant current pulses were applied between action potentials and during the plateau potential to determine if there were a decrease in membrane slope resistance during the plateau. It was found that the amplitude of the electrotonic potential recorded during the plateau was significantly less than the amplitude of the electrotonic potential recorded between action potentials. 6. The rate of repolarization of the plateau potential was studied in normal Krebs solution and in 2 mM-TEA Krebs solution. The rate of repolarization of the plateau potential was slowed in TEA Krebs solution. 7. It is concluded that there is an increase in the membrane conductance during the plateau potential. The repolarization following the plateau potential is due to a TEA-sensitive outward current.

Action Potentials↗

PubMed1981

Adriamycin induced alterations in canine Purkinje fiber action potential.

To study the electrophysiologic effects of adriamycin, transmembrane action potential characteristics of canine purkinje fibers were analyzed. Adriamycin significantly (p less than 0.05) prolonged action potential duration and refractory period but did not significantly alter resting membrane potential, action potential amplitude, dV/dt max and threshold for stimulation. Furthermore adriamycin effects were not reversible 20 minutes after the drug had been 'washed out'. These data indicate that adriamycin has significant cardiac electrophysiology effects that may account for its toxicity in man and that these effects are not quickly reversible.

Action Potentials↗

PubMed1999

Neuromodulation of dendritic action potentials.

The extent to which regenerative action potentials invade hippocampal CA1 pyramidal dendrites is dependent on both recent activity and distance from the soma. Previously, we have shown that the amplitude of back-propagating dendritic action potentials can be increased by activating either protein kinase A (PKA) or protein kinase C (PKC) and a subsequent depolarizing shift in the activation curve for dendritic K+ channels. Physiologically, an increase in intracellular PKA and PKC would be expected upon activation of beta-adrenergic and muscarinic acetylcholine receptors, respectively. Accordingly, we report here that activation of either of these neurotransmitter systems results in an increase in dendritic action-potential amplitude. Activation of the dopaminergic neurotransmitter system, which is also expected to raise intracellular adenosine 3',5'-cyclic monophosphate (cAMP) and PKA levels, increased action-potential amplitude in only a subpopulation of neurons tested.

Action Potentials↗

PubMed1989

Repolarization interactions between cardiac segments of varying action potential duration.

We studied interactions between action potential duration (APD) disperse zones using a double compartment bath in which an APD lengthening solution (Ni++ 2 mmol/L, in Tyrode's solution) was added to one compartment (which contained a portion of the fiber labeled "segment A") followed by addition of an APD shortening solution (6 to 10 mmol/K+) to the other compartment ("segment B"). Standard microelectrode techniques were used in canine Purkinje fibers. With Ni++ in segment A, there was a dispersion in APD measured at both 50% (APD50) and 95% (APD95) of repolarization. After selective addition of K+ to segment B, APD50 dispersion remained constant while APD95 dispersion increased, which indicated a change in the slope of repolarization, a factor with possible arrhythmogenic potential. In addition, a characteristic transitional action potential was seen adjacent to the partition. This had a timely and normally sloping early repolarization followed by a much more gradually sloping shelf. Premature action potentials arising during this shelf had diminished upstrokes. Results of these experiments may be useful in evaluating APD dispersion in relation to arrhythmias.

Action Potentials↗

PubMed1982

Synaptic inputs and action potentials of magnocellular neuropeptidergic cells: intracellular recording and staining in slices of rat hypothalamus.

Excitatory postsynaptic potentials (EPSPs) and action potentials of magnocellular neuropeptidergic cells (MNCs) in the paraventricular (PVN) and supraoptic nuclei (SON) were studied with intracellular recording in coronal slices of rat hypothalamus. The fluorescent dye Lucifer Yellow (LY) was injected intracellularly and the cells were subsequently identified as magnocellular (somata greater than 15 x 15 micrometer). These cells generally had a large cytoplasm-to-nucleus ratio. In PVN it was frequently possible to trace filled dendrites to the ependyma of the third ventricle, and occasionally dendritic spines could be seen. Electrical stimuli in areas dorsolateral and ventrolateral to the fornix column evoked EPSPs in some anatomically identified MNCs of PVN, which indicates that presynaptic fibers innervating MNCs approach PVN from this region. Short-latency (less than 1 msec) spikes could be evoked in many MNCs of PVN by stimulation near SON, which is consistent with the known projection to the neurohypophysis of many MNCs. Action potentials in MNCs of PVN and SON had significantly longer durations at one-third spike height (mean +/- S.D. = 2.06 +/- 0.6 msec) than hippocampal CA1 pyramidal cells (1.17 +/- 0.29 msec). This suggests that neuroendocrine cells in mammals and some lower vertebrates and invertebrates are similar in this regard.

Action Potentials↗

PubMed2002

Effects of current and potential dental etchants on nerve compound action potentials.

In this study, a 35% phosphoric acid gel (3M Scotchbond etchant), a nonrinse etchant (NRC), and two EDTA-containing conditioners (RC-Prep and File-Eze) were tested in vitro for blocking nerve conductance evoked in the rat sciatic nerve after local application. The phosphoric acid gel and NRC completely and irreversibly inhibited conductance. On the other hand, RC-Prep reduced the compound action potentials (cAPs) by 50% in 120 min. With File-Eze, the reduction in cAPs was less than 50% after an application time of 160 min (61.8 +/- 1.8%). At 160 min the cAPs in the RC-Prep group had been inhibited by 62.4%. These results indicated strong neurotoxic effects of phosphoric acid and NRC when applied directly on exposed pulp in the total etch procedure.

Acid Etching, Dental↗

PubMed1992

A numerical reconstruction of the effects of late stimulation on a cardiac ventricular action potential.

Numerical simulations of a propagating cardiac action potential utilizing Beeler-Reuter and Drouhard-Roberge physiological routines for the membrane current have been performed. These action potentials show increases in action potential duration when subjected to strong late stimuli of either positive or negative polarity. The mechanism is the same as that reported in an earlier paper which utilized a different physiological approach: repolarizing stimuli can reset the fast sodium gates locally so that they can be retriggered by diffusive return of charge from surrounding tissue. This results in a large depolarizing transient that lengthens action potential duration.

Action Potentials↗

PubMed1986

Dorsal horn potentials and current source densities evoked by single action potentials in single slowly adapting type I axons.

The slow-wave response of cat dorsal horn, elicited by single action potentials in single slowly adapting type I (SAI) axons, was mapped by averaging the slow wave recorded from each locus in a rectangular array of recording loci in the transverse plane. Current source-density (CSD) waveforms were computed from these averages. Evoked potentials always included N-waves, with mean latency = 4.9 ms, rise time (base line to peak) = 2.3 ms, and duration (base line-peak-base line) = 13.1 ms. In some planes, the N-wave was followed by a longer P-wave. The N-wave timing corresponded to previously described excitatory postsynaptic potentials (EPSPs) recorded intracellularly and excitatory discharges recorded extracellularly from single units evoked by single SAI spikes. The P-wave timing corresponded to a previously described postexcitatory suppression of SAI spike-evoked EPSPs and discharges following single conditioning SAI action potentials. The current sink during the N-wave had the following properties: It occurred in a column of tissue, perpendicular to the laminar borders, less than 600 microns wide; this is similar to the terminal domain of a single SAI collateral. It remains stationary during the N-wave, indicating that the excited population of dorsal horn elements does not spread or shift within the transverse plane during the response. It is somatotopically organized in the mediolateral dimension, in a manner similar to the somatotopic organization of primary afferent terminations and of dorsal horn cell receptive fields.

Action Potentials↗

PubMed2001

Dichotomy of action-potential backpropagation in CA1 pyramidal neuron dendrites.

In hippocampal CA1 pyramidal neurons, action potentials are typically initiated in the axon and backpropagate into the dendrites, shaping the integration of synaptic activity and influencing the induction of synaptic plasticity. Despite previous reports describing action-potential propagation in the proximal apical dendrites, the extent to which action potentials invade the distal dendrites of CA1 pyramidal neurons remains controversial. Using paired somatic and dendritic whole cell recordings, we find that in the dendrites proximal to 280 microm from the soma, single backpropagating action potentials exhibit <50% attenuation from their amplitude in the soma. However, in dendritic recordings distal to 300 microm from the soma, action potentials in most cells backpropagated either strongly (26-42% attenuation; n = 9/20) or weakly (71-87% attenuation; n = 10/20) with only one cell exhibiting an intermediate value (45% attenuation). In experiments combining dual somatic and dendritic whole cell recordings with calcium imaging, the amount of calcium influx triggered by backpropagating action potentials was correlated with the extent of action-potential invasion of the distal dendrites. Quantitative morphometric analyses revealed that the dichotomy in action-potential backpropagation occurred in the presence of only subtle differences in either the diameter of the primary apical dendrite or branching pattern. In addition, action-potential backpropagation was not dependent on a number of electrophysiological parameters (input resistance, resting potential, voltage sensitivity of dendritic spike amplitude). There was, however, a striking correlation of the shape of the action potential at the soma with its amplitude in the dendrite; larger, faster-rising, and narrower somatic action potentials exhibited more attenuation in the distal dendrites (300-410 microm from the soma). Simple compartmental models of CA1 pyramidal neurons revealed that a dichotomy in action-potential backpropagation could be generated in response to subtle manipulations of the distribution of either sodium or potassium channels in the dendrites. Backpropagation efficacy could also be influenced by local alterations in dendritic side branches, but these effects were highly sensitive to model parameters. Based on these findings, we hypothesize that the observed dichotomy in dendritic action-potential amplitude is conferred primarily by differences in the distribution, density, or modulatory state of voltage-gated channels along the somatodendritic axis.

Action Potentials↗

PubMed1990

Ionic dependencies of tetrodotoxin-resistant action potentials in trigeminal root ganglion neurons.

Action potentials recorded in vitro from the perikarya of trigeminal root ganglion neurons (guinea-pig) were examined for their sensitivities to blockers of specific ion channels or to removal of certain ionic species in the bathing media. The majority (approximately 65%) of the 137 neurons exhibited action potentials following application of the Na(+)-channel blocker, tetrodotoxin. This group of neurons was selected for further investigation under conditions of extracellular K(+)-channel blockade with tetraethylammonium and 4-aminopyridine. Long-duration action potentials consisting of two distinct components could be evoked under such conditions. The fast component of the spike was abolished in Na(+)-deficient perfusion media and was sensitive to blockade by extracellular lidocaine or intracellular QX-222 applications. It is likely that the slow component was mediated mainly by Ca2+, but in Ca2(+)-deficient media. Mg2(+)-influx may have contributed to the small voltage response. The amplitude and shape of the slow component was unaffected by applications of lidocaine or QX-222. Self-sustained repetitive firing was also observed in 11 neurons in the above conditions. This activity persisted even under conditions of severe deficiencies in extracellular [Ca2+] or [Na+]. Two distinct but overlapping K(+)-conductances that were sensitive to blockade by internal Cs(+)-application and insensitive to applications of tetraethylammonium and 4-aminopyridine, appear to mediate the afterhyperpolarization of the long-duration spike. One portion of the afterhyperpolarization was 60-150 ms in duration and was unaffected by removal of Ca2+ from the extracellular media, while the other had a time-course lasting 150-250 ms and was abolished by removal of external Ca2+. In some neurons, these K(+)-conductances were blocked by high doses of doxorubicin or cisplatin. The results show that at least two ion species (Na+ and Ca2+) contribute to the formation of the tetrodotoxin-resistant, long-duration action potential in trigeminal root ganglion neurons during selective K(+)-conductance blockade and also provide evidence for Mg2+ involvement in the generation of this voltage response.

4-Aminopyridine↗

PubMed2001

Subthreshold inactivation of Na+ and K+ channels supports activity-dependent enhancement of back-propagating action potentials in hippocampal CA1.

Back-propagating action potentials in CA1 pyramidal neurons may provide the postsynaptic dendritic depolarization necessary for the induction of long-term synaptic plasticity. The amplitudes of back-propagating action potentials are not all or none but are limited in amplitude by dendritic A-type K+ channels. Previous studies of back-propagating action potentials have suggested that prior depolarization of the dendritic membrane reduces A-type channel availability through inactivation, resulting in an enhanced, or boosted, dendritic action potential. However, inactivation kinetics in the subthreshold potential range have not been directly measured. Furthermore, the corresponding rates of Na+ channel inactivation with depolarization have not been considered. Here we report in cell-attached patches (150-220 microm from the soma, 32 degrees C) that at 20-mV positive to rest, A-type K+ channels inactivated with a single exponential time constant of 6 ms, whereas Na+ channels inactivated with a time constant of 37 ms. The ratio of available Na+ to K+ current increased as the duration of the depolarization increased. Thus the subthreshold properties of Na+ and A-type K+ channels provide a mechanism by which information about the level of synaptic activity may be encoded in the amplitude of back-propagating action potentials.

Action Potentials↗

PubMed1995

Arrhythmia and delayed recovery of cardiac action potential during reperfusion after ischemia. Role of oxygen radical-induced no-reflow phenomenon.

The role of reactive metabolites of oxygen, oxygen radicals (O-Rs), as mediators of potentially arrhythmogenic alterations in cellular electrical properties and contractile dysfunction of cardiac muscle during reperfusion after ischemia was investigated. Electrical and mechanical activities of arterially perfused guinea pig right ventricular walls were recorded simultaneously with intracellular microelectrodes and a force transducer. Preparations were maintained in Krebs-Henseleit solution (perfusion rate, 1.5 mL/min) and subjected to 30 minutes of no-flow ischemia followed by 60 minutes of reperfusion or pretreated with O-R scavengers (superoxide dismutase, 50 U/mL; catalase, 600 U/mL; and mannitol, 2 mmol/L) for 10 to 20 minutes, followed by 30 minutes of ischemia and 60 minutes of reperfusion. Reperfusion in untreated preparations caused (1) depolarization of resting membrane potential by 8 to 10 mV and slow recovery of action potential duration requiring 60 minutes to attain the preischemic duration, (2) tachyarrhythmias and premature action potentials, (3) postischemic contractile dysfunction, and (4) increased coronary perfusion pressure in untreated preparations. Pretreatment with scavenger cocktail affected neither electrical nor contractile activity before or during no-flow ischemia, but it (1) accelerated recovery of resting membrane potential and action potential duration, (2) reduced the incidence of tachyarrhythmia, (3) improved contractile function, and (4) inhibited the rise in perfusion pressure on reflow. Reperfusion with an exogenous O-R-generating system containing xanthine/xanthine oxidase (X/XO, 2 mmol/L:10 mU/mL) inhibited recovery of action potential duration and contractility. Treatment of normoxic arterially perfused right ventricular walls with X/XO caused a decline in action potential duration by approximately 20% within 30 minutes. In contrast, X/XO caused a 30% increase in the duration of action potentials in superfused papillary muscles or small strips of right ventricular walls over the same time period. Pretreatment with sodium nitroprusside (10 mumol/L) inhibited the decline in duration induced by X/XO in normoxic right ventricular walls but was without effect on prolongation due to X/XO in papillary muscles. Reperfusion with nitroprusside after no-flow ischemia caused (1) accelerated recovery of preischemic action potential configuration, (2) a significant decline in the incidence of reperfusion arrhythmias, (3) improved postischemic contractile performance, and (4) inhibition of the increase in perfusion pressure associated with reflow. The data indicate that slow recovery of the action potential duration caused by O-Rs in reperfusion cannot be explained by the direct effects of O-Rs on cardiac myocytes.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗