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PubMed1999

Action potentials that mimic fibrillation activate sodium current.

Ventricular fibrillation (VF) has brief action potentials (50-70 ms) with short diastolic intervals (10-30 ms). Under these conditions ion channel activity may be grossly different to normal sinus rhythm (NSR). In particular, sodium channel activation may not contribute to the generation and propagation of action potentials during VF. This study determined if sodium channels can be activated when action potentials mimic VF. Isolated chick ventricular myocytes (n=7) were voltage-clamped to quantitate fast inward sodium current. The voltage clamp protocol simulated VF with a 10 pulse train at 10 Hz (100 ms cycle length (CL)) and depolarization interval (action potential duration) ranging from 90 to 20 ms. After each train a test pulse was delivered from holding (-80 mV) in 10-ms steps. The train preceded each step pulse. Peak sodium current for control and each VF protocol occurred at a membrane potential (V(m)) of -10 mV. Sodium current was evident during brief resting intervals as short as 20 ms, albeit 10-20% of baseline. Resting intervals less than 60 ms shifted the sodium conductance activation curve from Vm(0.5)-30 mV to -22 mV membrane potential. Similar findings occurred when resting potential was at -65 mV, although there was less sodium current with all tested protocols. There was significantly less inactivation of sodium current when the prepulse was shorter (100 v 1000 ms). There was approximately 20% greater sodium current when the test pulse followed a short v long depolarized (>-80 mV) prepulse. Although the longer depolarization pulses produce approximately 20% greater sodium current at membrane potentials more negative than -80 mV. Lastly the time for half recovery of sodium current from activation was significantly less when the inactivating prepulse was short v long (45.9+/-9 v 118+/-20 ms, P<0.05). In conclusion, sodium current is evident when the diastolic rest interval is as brief as 10-20 ms. Rest interval, length of membrane depolarization and membrane potential interact to affect sodium channel activation, inactivation and recovery from inactivation. These data demonstrate that the brief action potentials at more depolarized membrane potentials seen during VF allow for inward sodium current upon depolarization, less sodium channel inactivation, and a faster recovery from inactivation, thereby compensating for a short diastolic rest interval. Therefore, it is likely that the inward sodium channel contributes to wave front propagation during ventricular fibrillation.

Action Potentials↗

PubMed1998

Information transmission at 500 bits/s by action potentials in a mechanosensory neuron of the cockroach.

Action potentials are widely used to transmit information within nervous systems but information encoding and transmission rates by action potentials are poorly understood. In the absence of knowledge about encoding, most previous work has used signal-to-noise ratios to estimate information capacities. We used a mechanosensory neuron to transmit information by a simple encoding scheme that allowed us to measure the transmission rate directly. Using either mechanical or electrical stimulation, information was transmitted at rates up to 500 bits/s, higher than ever reported before for real action potentials. However, the maximum possible message length decreased strongly with transmission rate, from approximately infinite at 100 bits/s to approximately 100 ms at 500 bits/ s, probably due to ionic adaptation processes within the neuronal membrane.

Action Potentials↗

PubMed1983

Concentration-dependent effect of trapidil on slow action potentials in cardiac muscle.

Trapidil, a coronary vasodilator and positive inotropic agent, was tested for its ability to affect the normal "fast" action potentials and the "slow" action potentials and contractions of isolated perfused chick hearts, and to affect the tissue cyclic AMP level. At 5 X 10(-3) M, trapidil completely blocked the fast Na+ channels in hearts perfused with normal Tyrode solution, since this dose abolished the action potential when verapamil (2 X 10(-6) M) was present to eliminate the inward slow current. To study effects on the slow channels, the fast Na+ channels were voltage-inactivated by partial depolarization to about -40 mV with an elevated (25 mM) K+-Tyrode solution, resulting in loss of excitability. At low concentrations (1 X 10(-4) - 1 X 10(-3) M), trapidil induced slow action potentials accompanied by contractions, even in the presence of a beta-adrenergic blocker. In contrast, at high concentrations (3 X 10(-3) - 1 X 10(-2) M), trapidil markedly depressed or blocked the isoproterenol-induced slow action potentials. Consistent with this dual action, in hearts perfused with normal Tyrode solution, trapidil exerted a small positive inotropic action at low doses and a considerable negative inotropic action at high doses, even though the intracellular cyclic AMP level was substantially elevated. That is, trapidil has actions similar to those of papaverine. It is concluded that trapidil blocks both fast Na+ channels and slow channels in cardiac muscle, the fast Na+ channels being more sensitive, and that low concentrations of trapidil induce slow channels by elevating the cyclic AMP level because of phosphodiesterase inhibition.

Action Potentials↗

PubMed1998

Synaptic regulation of action potential timing in neostriatal cholinergic interneurons.

Action potentials in neostriatal cholinergic interneurons recorded in vivo are triggered by summation of two or three discrete synaptic depolarizations (Wilson et al., 1990). The ability and precision with which EPSPs and IPSPs regulate action potential timing was therefore investigated in vitro. Cholinergic interneurons were identified on the basis of morphological and electrophysiological characteristics in neostriatal slices taken from 2- to 3-week-old postnatal rats recorded at 24-26 degreesC. During periods of induced regular firing, intrastriatal stimuli were used to evoke pharmacologically isolated monosynaptic AMPA receptor-mediated EPSPs or GABAA receptor-mediated IPSPs. EPSPs evoked during the interspike interval (ISI) produced a phase-dependent decrease in the ISI, whereas IPSPs produced a phase-independent prolongation of the ISI. Injection of brief depolarizing currents mimicked the action of EPSPs and revealed an alteration in the input resistance during the ISI. In contrast to IPSPs, the ability of brief hyperpolarizing current injections to delay spike generation was phase-dependent. After blockade of GABAergic and glutamatergic synaptic transmission, stimuli failed to produce a detectable conductance change but could still prolong the subsequent ISI primarily through a D1 dopamine receptor-mediated enhancement of the afterhyperpolarization (AHP). Hence, EPSPs are ideally suited to provide a precise regulation of spike timing in cholinergic cells, whereas IPSPs are more likely to influence the overall level of excitability. The D1-mediated modulation of the AHP may contribute to the prolonged ISI seen in tonically active neurons in vivo in monkeys trained to respond to a sensory cue.

2-Amino-5-phosphonovalerate↗

PubMed1998

Presynaptic afferent inhibition of lobster olfactory receptor cells: reduced action-potential propagation into axon terminals.

Action-potential propagation into the axon terminals of olfactory receptor cells was measured with the use of voltage-sensitive dye imaging in the isolated spiny lobster brain. Conditioning shocks to the olfactory nerve, known to cause long-lasting suppression of olfactory lobe neurons, allowed the selective imaging of activity in receptor cell axon terminals. In normal saline the optical signal from axon terminals evoked by a test stimulus was brief (40 ms) and small in amplitude. In the presence of low-Ca2+/high-Mg2+ saline designed to reduce synaptic transmission, the test response was unchanged in time course but increased significantly in amplitude (57 +/- 16%, means +/- SE). This increase suggests that propagation into receptor cell axon terminals is normally suppressed after a conditioning shock; this suppression is presumably synaptically mediated. Thus our results show that presynaptic inhibition occurs at the first synapse in the olfactory pathway and that the inhibition is mediated, at least in part, via suppression of action-potential propagation into the presynaptic terminal.

Action Potentials↗

PubMed1999

Detecting single fiber contributions to motor unit action potentials.

The ability to detect muscle fiber action potential (MFAP) contributions to motor unit action potentials (MUAPs) measured using single fiber (SF) and concentric needle (CN) electrodes was studied using simulated MUAPs. Various MFAP-acceleration thresholds were used to define significant fiber contributions. Attempts to detect the significant MFAP contributions, by locating peaks in filtered MUAPs or MUAP accelerations using various MUAP-based thresholds, were then made. Considering filtered MUAPs and a significant contribution threshold of 7.5 kV/s2, and using fiber-density peak-detection criteria, at best 46% and 50% of significant MFAP contributions were detected for the SF and CN MUAPs, respectively. Considering MUAP accelerations and a significant contribution threshold of 7.5 kV/s2, 80% and 84% of significant MFAP contributions could be detected, respectively. Most significant contributions were created from fibers located within approximately 350 microm of the electrode. The results suggest that significant peaks, defined using MUAP-based thresholds, within the acceleration of CN MUAPs can strongly correspond to individual fiber activity and may be useful for measuring fiber density and neuromuscular jitter.

Action Potentials↗

PubMed1986

The action potential of guinea pig bladder smooth muscle.

The smooth muscle of the guinea pig bladder demonstrates in vitro spontaneous electrical activity in the form of action potentials which are associated with contraction. The action potential frequency is highly voltage-sensitive. The relative contributions of Na, Ca and K to the action potential elicited by depolarizing current have been studied using intracellular microelectrodes. In solutions in which NaCl is replaced by sucrose, the membrane hyperpolarizes and the rate of rise and after-hyperpolarization of the elicited action potential is increased. The amplitude is unaffected. In Ca-deficient solutions, the membrane depolarizes, the rate of rise and amplitude of the action potential is reduced, and the after-hyperpolarization is decreased. Nifedipine reduces amplitude and rate of rise but does not affect after-hyperpolarization. In the presence of the K-channel antagonist TEA, the duration of the action potential is prolonged, but the amplitude and rate of rise are unaffected. After-hyperpolarization is not reduced. It is concluded that the action potential of guinea pig bladder muscle, like many other smooth muscles studied, is Ca-based. Repolarization depends on changes in K conductance. The after-hyperpolarization is voltage-sensitive.

Action Potentials↗

PubMed1986

Effects of pineal factors on the action potentials of sympathetic neurons.

Neurons from rat superior cervical ganglia were grown in coculture with pineal cells. Action potentials of neurons in cocultures were 25% longer and were 25% greater in amplitude than those recorded from neurons grown in the presence of ganglionic nonneuronal cells alone. Neurons showed an increase in action potential duration with increasing time in culture. This may have been related to the recovery of nonneuronal cell populations after an initial exposure to the antimitotic agent Ara-C. In cultures not initially exposed to Ara-C, a subsequent exposure after 7 days in culture resulted in a shortening of the action-potential duration. Neuronal cultures were exposed to gel slabs containing the pineal indolamines, serotonin, N-acetylserotonin, and melatonin. Serotonin and N-acetylserotonin showed no effect on the neuronal action potentials at the concentrations tested. Melatonin caused an increase in action-potential duration that was associated not with an increase in action-potential amplitude, but with a decrease in action-potential rise rates. The effects of long-term exposure in melatonin appeared to be reversible in some cells but not in all. Short-term effects of melatonin were observed in older cultures and in younger cultures after the cells were stimulated repeatedly. Older cultures also had higher levels of spontaneous activity. The dependence of the short-term effects of melatonin on electrical activity may suggest a role for melatonin as a neuromodulator.

Action Potentials↗

PubMed1979

Propagation of action potentials in squid giant axons. Repetitive firing at regions of membrane inhomogeneities.

Effects of reduction in potassium conductance on impulse conduction were studied in squid giant axons. Internal perfusion of axons with tetraethylammonium (TEA) ions reduces G K and causes the duration of action potential to be increased up to 300 ms. This prolongation of action potentials does not change their conduction velocity. The shape of these propagating action potentials is similar to membrane action potentials in TEA. Axons with regions of differing membrane potassium conductances are obtained by perfusing the axon trunk and one of its two main branches with TEA after the second branch has been filled with normal perfusing solution. Although the latter is initially free of TEA, this ion diffuses in slowly. Up until a large amount of TEA has diffused into the second branch, action potentials in the two branches have very different durations. During this period, membrane regions with prolonged action potentials are a source of depolarizing current for the other, and repetitive activity may be initiated at transitional regions. After a single stimulus in either axon region, interactions between action potentials of different durations usually led to rebound, or a short burst, of action potentials. Complex interactions between two axon regions whose action potentials have different durations resembles electric activity recorded during some cardiac arrhythmias.

Action Potentials↗

PubMed1986

[The influence of the rapid rise of intraluminal pressure of the upper urinary tract on ureteral action potentials].

The present investigation was undertaken in order to examine the ureteral action potentials following transient rapid rise of the intraureteral pressure. In 21 adult mongrel dogs, physiological saline and 5% formalin were injected into the left and right obstructed ureters, respectively to produce rapid rise of intraureteral pressure to 60 cmH2O for 7 minutes, and then ureter was released from obstruction. In these experiments, recordings of ureteral electromyogram and intraureteral pressure were made. Histological changes of pelvi-ureteral system were also observed microscopically. Results 1. After injection of physiological saline, discharge intervals were significantly shortened, but normal discharge intervals were restored when the ureters were released from obstruction. Under conditions of reobstruction, the discharge intervals were shortened and intraureteral pressure inducing the shortest discharge interval was 50 cmH2O. 2. After injection of formalin, discharge intervals were significantly shortened, and the action potentials disappeared in 1 minute 28 seconds to 4 minutes 51 seconds after the injection in 18 out of the 21 ureters. No discharge was observed at 7 minutes after the injection in 16 out of the 18 ureters. In 14 out of the 16 ureters, however, the action potentials were restored when the ureters were released from obstruction or after the obstruction was readministered. Under conditions of reobstruction, discharge intervals were shortened, and intraureteral pressure inducing the shortest discharge interval was 20 cmH2O. 3. Histologically, the loss of epithelium, as well as edema and vasodilatation in lamina propria, were observed only in the mucosa of the middle portion of the ureters receiving formalin. The results of the present study show that a transient rapid rise of intraluminal pressure of the upper urinary tract caused by the injection of physiological saline or formalin, dose not have a significant effect on the ureteral action potentials, and that disappearance of the action potentials is refered to pharmacological action of formalin.

Action Potentials↗

PubMed1999

Augmentation and suppression of action potentials by estradiol in the myometrium of pregnant rat.

The purpose of this study was to investigate the actions of estradiol on spontaneous and evoked action potentials in the isolated longitudinal smooth muscle cells of the pregnant rat. Single cells were obtained by enzymatic digestion from pregnant rat longitudinal myometrium. Action potentials and currents were recorded by whole-cell current-clamp and voltage-clamp methods, respectively. The acute effects of 17beta-estradiol on action potentials and inward and outward currents were investigated. The following results were obtained. The average resting membrane potential of single myometrial cells was -54 mV (n = 40). In many cells, an electrical stimulation evoked a membrane depolarization, and action potentials were superimposed on the depolarization. In some cells, spontaneous action potentials were observed. Estradiol (30 microM) slightly depolarized the membrane (ca. 5 mV) and attenuated the generation of action potentials by reducing the frequency and amplitude of the spikes. Afterhyperpolarization was also attenuated by estradiol (30 microM). On the other hand, in 5 of 35 cells, estradiol increased the first spike amplitude and action potential duration, while frequency of the spike generation and afterhyperpolarization were inhibited. In voltage-clamped muscle cells, estradiol inhibited both inward and outward currents. Acute inhibition or augmentation of spike generation by estradiol is due to the balance of inhibition of inward and outward currents. Inhibition of both currents also prevented afterhyperpolarization, causing potential-dependent block of Ca spikes.

Action Potentials↗

PubMed1988

Presynaptic Na/Ca action potentials in unmyelinated axons of olfactory cortex.

(1) Pial surface slices of guinea-pig olfactory cortex were cut to have a thickness of 150 micron. Action potentials were recorded from the sectioned ends of the unmyelinated afferent axons originating from the lateral olfactory tract (LOT). These potentials were prolonged by the K-channel blocker 3,4-diaminopyridine (0.1 mmol/l) and further lengthened by tetraethylammonium (10 mmol/l). The action potential was also greatly prolonged by partly replacing the K+ in the bathing solution by Cs+. (2) These prolonged action potentials were shortened by Cd2+; Gd3+ (gadolinium); Ni2+; Mn2+; Co2+, in order of potency. The residual early component of the action potential was tetrodotoxin (TTX) sensitive. In contrast, the LOT action potential was little affected by Ca-channel blockade. (3) Organic Ca-channel blockers either had no effect (0.05 mmol/l nifedipine), or depressed the early and later phases of the prolonged action potential equally (0.05-0.5 mmol/l verapamil or 0.05-0.2 mmol/l diltiazem). (4) A propagated action potential was also obtained in solution containing TTX and low Na+. This potential was supported by Ca2+, Sr2+ or Ba2+ and completely suppressed by Cd2+. (5) The later parts of the action potential, after K-channel blockade, had a pharmacological sensitivity towards Ca-channel blockers matching that of synaptic transmission. This suggests the falling phase of the action potential is caused by charge carrier (mainly Ca2+) passing through Ca-channels that have similar properties to, or are the same as those which open prior to transmitter release.

4-Aminopyridine↗

PubMed1986

[Importance of intraoperative monitoring of ABR and compound action potential of the eighth cranial nerve during microvascular decompression surgery].

An intraoperative recording of a direct compound action potential of the 8th cranial nerve with pre, intra and postoperative monitorings of auditory brainstem evoked response (ABR) was carried out for the purpose of clarifying mechanism and prevention of postoperative hearing dysfunction following microvascular decompression surgery as a treatment for hyperdysfunction syndrome of cranial nerves. In 221 patients with hemifacial spasm and tic douloureux out of 510 patients operated on by microvascular decompression surgery, ABR was monitored before, during and after surgery and furthermore, in the recent 94 patients among them, an intraoperative direct recording of a compound action potential of the acoustic nerve was performed simultaneously. Among these 94 patients, postoperative mild hearing dysfunction was encountered in 11 patients and severe reduction of hearing acuity in 2. As a result of our studies of monitoring action potential of the 8th cranial nerve and ABR, the following conclusions were drawn. When a latency of component V of ABR was delayed by more than 1.5-2.0 msec during surgery, and delay of latency of main negative peak (N1) of an action potential of the acoustic nerve exceeded by more than 1.0 msec, the occurrence rate of postoperative hearing dysfunction became positively high. There were two different types of changes in both ABR and action potentials; one type was a delay of an action potential in combination with that of ABR latencies and the other one was merely a delay in ABR components without following a remarkable change in action potentials. The former change might due to be an insult of whole neural pathways of the 8th cranial nerve including a cochlear nucleus and the latter change may due to be functional changes of the structures proximal to the cochlear nucleus. The delay of latencies in ABR and action potentials could be imposed either by a traction of the 8th cranial nerve or by a compression of the region of cochlear nucleus by a blain spatula as well as a vascular insufficiency of the tiny vessels which supplied these neural structures. To avoid the surgical insult to the acoustic nerve itself and more proximal neural pathways, the traction of any neural structures by a brain spatula should be lasted less than 5 minutes with more than 2 minutes intervals when judged from the results of our monitoring studies and the pressure of the compression on the cerebellar cortex is much preferable to be less than 20 mmHg for the safety throughout whole surgical procedures.

Adult↗

PubMed2003

Sympathetic activity and the underlying action potentials in sympathetic nerves: a simulation.

Understanding the relationship between activity recorded in sympathetic nerves and the action potentials of the axons that contribute to that activity is important for understanding the processing of sympathetic activity by the central nervous system. Because this relationship cannot be determined experimentally and is difficult to predict analytically, we simulated the summed action potentials of 300 axons. This simulation closely resembled actual sympathetic activity and permitted us to know how many action potentials contributed to each burst of simulated sympathetic activity and the durations and amplitudes of each burst. We used these simulated data to examine a statistical method (cluster analysis) that has been used to identify and quantify bursts of sympathetic activity. Simulation indicated that the integrals of bursts, whether determined directly from the simulation or by integrating bursts detected by cluster analysis, were linearly correlated to the number of action potentials contributing to bursts. The variances of samples of the simulated signal were also linearly correlated to the number of action potentials. The amplitudes of bursts of sympathetic activity were less well correlated to the number of underlying action potentials. A linear relationship existed between the average number of action potentials contributing to simulated bursts and the integral of the amplitude spectra obtained by Fourier transform of the simulated activity. Finally, simulated experiments indicated that relatively brief recordings might be sufficient to detect statistically significant changes in sympathetic activity.

Action Potentials↗

PubMed1997

Electrophysiologic effects of acute myocardial ischemia: a theoretical study of altered cell excitability and action potential duration.

OBJECTIVE: To study the ionic mechanisms of electrophysiologic changes in cell excitability and action potential duration during the acute phase of myocardial ischemia. METHODS: Using an ionic-based theoretical model of the cardiac ventricular cell, the dynamic LRd model, we have simulated the three major component conditions of acute ischemia (elevated [K]o, acidosis and anoxia) at the level of individual ionic currents and ionic concentrations. The conditions were applied individually and in combination to identify ionic mechanisms responsible for reduced excitability at rest potentials, delayed recovery of excitability, and shortened action potential duration. RESULTS: Increased extracellular potassium ([K]o) had the major effect on cell excitability by depolarizing resting membrane potential (Vrest), causing reduction in sodium channel availability. Acidosis caused a [K]o-independent reduction in maximum upstroke velocity, (dVm/dt)max. A transition from sodium-current dominated to calcium-current dominated upstroke occurred, and calcium current alone was able to sustain the upstroke, but only after sodium channels were almost completely (97%) inactivated. Acidic conditions prevented the transition to calcium dominated upstroke by acidic reduction of both sodium and calcium currents. Anoxia, simulated by lowering [ATP]i and activating the APT-dependent potassium current, IK(ATP), was the only process that could decrease action potential duration by more than 50% and reproduce AP shape changes that are observed experimentally. Acidic or anoxic depression of the L-type calcium current could not reproduce the observed action potential shape changes and APD shortening. Delayed recovery of excitability, known as 'post-repolarization refractoriness', was determined by the voltage-dependent kinetics of sodium channel recovery; Vrest depolarization caused by elevated [K]o increased the time constant of (dVm/dt)max recovery from tau = 10.3 ms at [K]o = 4.5 mM to tau = 81.4 ms at [K]o = 12 mM, reflecting major slowing of sodium-channel recovery. Anoxia and acidosis had little affect on tau. CONCLUSIONS: The major conditions of acute ischemia, namely elevated [K]o, acidosis and anoxia, applied at the ionic channel level are sufficient to simulate the major electrical changes associated with ischemia. Depression of membrane excitability and delayed recovery of excitability in the single, unloaded cell are caused by elevated [K]o with additional excitability depression by acidosis. Major changes in action potential duration and shape can only be accounted for by anoxia-dependent opening of IK(ATP).

Acidosis↗

PubMed1967

Permeability changes associated with the action potential in procaine-treated crayfish abdominal muscle fibers.

Permeability changes associated with prolonged action potentials have been analyzed in procaine-treated crayfish abdominal muscle fibers. The effect of external Ca indicates that the increase in membrane conductance observed during the rising phase of the action potential is primarily due to a permeability increase for Ca. A remnant of the permeability increase may cause the succeeding plateau as shown by its high conductance and by the effect of low Mn. A delayed increase in conductance precedes the termination of the plateau phase. This is due to a delayed increase in permeability, probably for K, that is observed when depolarizing electrogenesis is eliminated. High external Ca reduces the action potential duration, the falling phase starting at a higher depolarization. These changes may be related to an earlier onset of the delayed increase in permeability, induced by a larger inside positivity in the presence of higher Ca. No "anomalous rectification" is seen in early or late I-V curves for small depolarizations. Ba may replace Ca in its role in depolarizing electrogenesis, and the first action potential induced in Ba saline has a large overshoot and a long duration. In higher Ba salines, action potentials are greatly prolonged. Long term soaking in Rb-containing or K-free saline also augments and prolongs the action potential. These changes are assumed to be related to depression of the K permeability of the membrane.

Abdominal Muscles↗

PubMed1987

Action potential duration in ventricular muscle during selective metabolic block.

We have examined whether maintenance of the cardiac action potential duration depends exclusively on energy from glycolysis. Oxidative phosphorylation in guinea pig papillary muscles was inhibited by superfusion with hypoxic solutions. After 60 min in 50 mM glucose solution, the action potential duration was 85% of aerobic control, but ATP content was only 25%; after 60 min in 0 mM glucose, both the duration and ATP content had declined to 15% control. When the glucose concentration of hypoxic solution was raised from 0 to 50 mM, there was nearly full recovery of the action potential duration but ATP only increased to about 25% control. We attribute action potential shortening during metabolic inhibition to suppression of calcium current and activation of potassium current; the latter are graded in intensity and expressed only at low ATP. When normoxic muscle was treated with 20 mM 2-deoxy-D-glucose (2-DG) to inhibit glycolysis, there was an early transient shortening of the action potential. This was attributed to ATP consumption related to early rapid 2-DG influx and phosphorylation. After the transient, the action potential duration was maintained for several hours in oxygenated 2-DG solution. The duration was also maintained in oxygenated muscle depleted of glycolytic substrate. Thus we found no evidence of an exclusive relation between action potential duration and glycolysis.

Acetates↗

PubMed1985

Ionic basis of the different action potential configurations of single guinea-pig atrial and ventricular myocytes.

Single myocardial cells were enzymatically dispersed from guinea-pig atria and ventricles. At 25 degrees C, atrial cell action potentials differed significantly from ventricular cell action potentials in duration (atrial = 141 ms, ventricular = 497 ms) and over-shoot (atrial = +36 mV, ventricular = +42 mV). Action potentials of atrial and ventricular cells responded differently to changes in external K+ concentration ([K+]o). Elevation of [K+]o from 6 to 11 mM depolarized atrial cells but produced no significant change in action potential duration; similar changes in [K+]o depolarized ventricular cells and produced a significant shortening of the action potential duration. Voltage-clamp experiments were performed to investigate the ionic basis underlying the different action potential configurations of single atrial and ventricular myocytes. A single-micropipette voltage-clamp technique was used, employing either extremely small-tip diameter pipettes, without internal cell dialysis (Hume & Giles, 1983), or larger tip diameter pipettes, with internal dialysis (Hamill, Marty, Neher, Sakmann & Sigworth, 1981). Two significant differences in background K+ conductance in single atrial and ventricular myocytes were observed: (i) the isochronal (5 s) current-voltage relationship of single ventricular myocytes exhibited a region of prominent negative slope conductance and elevation of [K+]o produced cross-over; a negative slope conductance region was absent in atrial cells and elevation of [K+]o produced very little cross-over of isochronal current-voltage relationships, and (ii) hyperpolarizing voltage pulses applied from holding potentials of -50 mV elicited inward current in ventricular cells which decayed with time; similar voltage-clamp pulses in atrial cells elicited inward currents which fail to decay. Single K+ channel current measurements confirmed the existence of different resting K+ channel properties in single atrial and ventricular myocytes. Resting K+ channels in both cell types had similar single channel conductances (30-32 pS with [K+]o = 145 mM) but ventricular K+ channels had significantly slower gating kinetics compared to atrial K+ channels (ventricular K+ channel mean open time = 223 ms; atrial K+ channel mean open time = 1 ms at Vr (resting membrane potential) -20 mV). The plateau and duration of the guinea-pig ventricular action potential was insensitive to high concentrations of tetrodotoxin (3 X 10(-5) M) but extremely sensitive to external Ca2+ concentration ([Ca2+]o). The second inward Ca2+ current (iCa) density was estimated in small atrial and ventricular myocytes of similar diameter and length.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗