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PubMed1981

Relationship between the effects of Goniopora toxin on action potential and on contractile force in guinea-pig papillary muscle.

Effects of Goniopora toxin (GPT) on cardiac action potential and on contractile force were investigated in isolated guinea-pig papillary muscle. GPT produced a positive inotropic effect by increasing contractile force and prolonging the relaxation time. The time-to-peak force was little affected. GPT prolonged the action potential duration but did not affect the resting membrane potential nor the amplitude of the action potential. Thus there was a correlation between the positive inotropic effect and prolongation of the action potential duration. Tetrodotoxin or a reduction in extracellular sodium concentration attenuated both the positive inotropic effect and the prolonged duration of the action potential induced by GPT. Lanthanum or a reduction in extracellular calcium concentration also inhibited the increased contraction but did not shorten the prolonged durations of contraction and action potential. Verapamil attenuated the positive inotropic effect by reducing both the contractile force and the duration of contraction, but did not shorten the action potential duration. These results show that the positive inotropic effect of GPT depends on the increase in both sodium and calcium influxes while the prolonging effect on the action potential probably depends only on an increase in sodium influx. Hence, it is concluded that the prolongation of the action potential due to the increased sodium permeability is an essential process for the appearance of the positive inotropic effect of GPT.

Action Potentials↗

PubMed1986

Anthracycline-induced inhibition of a calcium action potential in differentiated murine neuroblastoma cells.

The effects of some anthracyclines on a Ca2+ -dependent action potential have been studied in differentiated murine neuroblastoma cells (N1E-115 clone). The differentiated neuroblastoma cell possesses characteristics of an electrically excitable cell and can generate propagated potential spikes in which Ca2+ is the inward charge carrier. This was shown by the fact that action potentials recorded from differentiated neuroblastoma cells in the presence of 10(-7) g of tetrodotoxin per ml, which inhibits active Na+ channels, had a spike amplitude that depended upon the extracellular Ca2+ concentration in a manner close to that predicted by the Nernst equation. The peak potential changed 28.9 mV/decade change in extracellular Ca2+. Local application to a cell of 10(-8) M doxorubicin produced inhibition of this Ca2+ -dependent action potential within 5 s of drug application and a maximum inhibition of 13% 60 s after drug application. There was almost complete recovery to the initial spike amplitude value within 10 min after removing drug. The same concentration of doxorubicin also produced complete inhibition, without recovery, of a Ca2+ -dependent after-discharge which followed the initial action potential in about half the cells studied. Increasing concentrations of doxorubicin produced dose-dependent inhibition of the initial Ca2+ -dependent action potential. Cells exposed to 10(-5) M doxorubicin showed 88% inhibition of the Ca2+ -dependent action potential with no recovery even 10 min after removing the drug. Daunomycin, 10(-6) M, produced 90% inhibition of the Ca2+ -dependent action potential. Daunomycin aglycone (10(-6) M), which lacks antitumor activity, had no significant effect on the Ca2+ -dependent action potential. The rapid onset of the drug-induced response together with the low concentrations of anthracyclines needed to inhibit voltage-dependent Ca2+ channels in the neuroblastoma cells suggest a direct effect of anthracyclines on the cell surface membrane. The findings are discussed in light of the possible role of Ca2+ in cancer cells.

Action Potentials↗

PubMed1999

Dendritic voltage-gated ion channels regulate the action potential firing mode of hippocampal CA1 pyramidal neurons.

The role of dendritic voltage-gated ion channels in the generation of action potential bursting was investigated using whole cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons located in hippocampal slices of adult rats. Under control conditions somatic current injections evoked single action potentials that were associated with an afterhyperpolarization (AHP). After localized application of 4-aminopyridine (4-AP) to the distal apical dendritic arborization, the same current injections resulted in the generation of an afterdepolarization (ADP) and multiple action potentials. This burst firing was not observed after localized application of 4-AP to the soma/proximal dendrites. The dendritic 4-AP application allowed large-amplitude Na(+)-dependent action potentials, which were prolonged in duration, to backpropagate into the distal apical dendrites. No change in action potential backpropagation was seen with proximal 4-AP application. Both the ADP and action potential bursting could be inhibited by the bath application of nonspecific concentrations of divalent Ca(2+) channel blockers (NiCl and CdCl). Ca(2+) channel blockade also reduced the dendritic action potential duration without significantly affecting spike amplitude. Low concentrations of TTX (10-50 nM) also reduced the ability of the CA1 neurons to fire in the busting mode. This effect was found to be the result of an inhibition of backpropagating dendritic action potentials and could be overcome through the coordinated injection of transient, large-amplitude depolarizing current into the dendrite. Dendritic current injections were able to restore the burst firing mode (represented as a large ADP) even in the presence of high concentrations of TTX (300-500 microM). These data suggest the role of dendritic Na(+) channels in bursting is to allow somatic/axonal action potentials to backpropagate into the dendrites where they then activate dendritic Ca(2+) channels. Although it appears that most Ca(2+) channel subtypes are important in burst generation, blockade of T- and R-type Ca(2+) channels by NiCl (75 microM) inhibited action potential bursting to a greater extent than L-channel (10 microM nimodipine) or N-, P/Q-type (1 microM omega-conotoxin MVIIC) Ca(2+) channel blockade. This suggest that the Ni-sensitive voltage-gated Ca(2+) channels have the most important role in action potential burst generation. In summary, these data suggest that the activation of dendritic voltage-gated Ca(2+) channels, by large-amplitude backpropagating spikes, provides a prolonged inward current that is capable of generating an ADP and burst of multiple action potentials in the soma of CA1 pyramidal neurons. Dendritic voltage-gated ion channels profoundly regulate the processing and storage of incoming information in CA1 pyramidal neurons by modulating the action potential firing mode from single spiking to burst firing.

4-Aminopyridine↗

PubMed1979

Relationships between peak force, action potential duration and stimulus interval in rabbit myocardium.

Isometric force and membrane action potential were recorded simultaneously in rabbit papillary muscles (36.5 degrees--37.5 degrees C). One to three test stimuli were given at various intervals (0.20--10.0 s) after a series of control contractions at constant stimulation intervals (1.0--1.5 s). Optimum peak force always occurred when the preceding test interval was 0.80 s. When this interval was greater than 0.80 s, time to peak force was a linear function of the action potential duration. Furthermore, under these conditions the action potential duration (AP1) and peak force (F1) of the test contraction could be used to predict peak force (F2) of the subsequent contraction elicited after a fixed interval (0.80--1.50 s) according to the equation (regression plane): F2 = BAPAP1 + BFF1 + A. Constants BAP and BF are interpreted to provide information about calcium influx during the action potential and of the recirculation of calcium between contractions, respectively. F2 deviated towards higher values than predicted from the equation when the preceding test contraction was triggered to occur at an interval less than 0.80 s. This may be due to an intensified calcium transport into the cell during the action potential after these short intervals. The action potential duration was inversely related to both the inotropic state of the muscle (representing a feed-back mechanism) and the preceding stimulation interval.

Action Potentials↗

PubMed2004

Reconstruction of action potential of repolarization in patients with congenital long-QT syndrome.

A method for reconstructing an action potential during the repolarization period was developed. This method uses a current distribution-plotted as a current-arrow map (CAM)--calculated using magnetocardiogram (MCG) signals. The current arrows are summarized during the QRS complex period and subtracted during the ST-T wave period in order to reconstruct the action-potential waveform. To ensure the similarity between a real action potential and the reconstructed action potential using CAM, a monophasic action potential (MAP) and an MCG of the same patient with type-I long-QT syndrome were measured. Although the MAP had one notch that was associated with early afterdepolarization (EAD), the reconstructed action potential had two large and small notches. The small notch timing agreed with the occurrence of the EAD in the MAP. On the other hand, the initiation time of an abnormal current distribution coincides with the appearance timing of the first large notch, and its end time coincides with that of the second small notch. These results suggest that a simple reconstruction method using a CAM based on MCG data can provide a similar action-potential waveform to a MAP waveform without having to introduce a catheter.

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PubMed2004

Monoamines increase the excitability of spinal neurones in the neonatal rat by hyperpolarizing the threshold for action potential production.

During fictive locomotion in the adult decerebrate cat, motoneurone excitability is increased by a hyperpolarization of the threshold potential at which an action potential is elicited (V(th)). This lowering of V(th) occurs at the onset of fictive locomotion, is evident for the first action potential elicited and is presumably caused by a neuromodulatory process. The present study tests the hypothesis that the monoamines serotonin (5-HT) and noradrenaline (NA) can hyperpolarize neuronal V(th). The neonatal rat isolated spinal cord preparation and whole-cell recording techniques were used to examine the effects of bath-applied 5-HT and NA on the V(th) of spinal ventral horn neurones. In the majority of lumbar ventral horn neurones, 5-HT (13/26) and NA (10/16) induced a hyperpolarization of V(th) ranging from -2 to -8 mV. 5-HT and NA had similar effects on V(th) for individual neurones. This hyperpolarization of V(th) was not due to a reduction of an accommodative process, and could be seen without changes in membrane potential or membrane resistance. These data reveal a previously unknown action of 5-HT and NA, hyperpolarization of V(th) of spinal neurones, a process that would facilitate both neuronal recruitment and firing.

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PubMed1999

Inhibitors of myosin light chain kinase block synaptic vesicle pool mobilization during action potential firing.

During repetitive action potential firing the maintenance of synaptic transmission relies on a continued supply of synaptic vesicles for fusion with the presynaptic plasma membrane. The mechanism of transport by which vesicles are delivered to the site of fusion from a reserve pool is unknown, as are the biochemical pathways linking intracellular Ca2+ elevation with vesicle mobilization. Here, using the fluorescent tracer FM1-43 in hippocampal synaptic terminals, I show that inhibitors of myosin light chain kinase can block mobilization of the reserve pool and not the immediately releasable pool.

Action Potentials↗

PubMed1996

Receiver operating characteristic (ROC) analysis of neural code efficacies. II. Optic nerve action potentials and neural transmission.

Action potentials (APs) were intracellularly recorded from eccentric cells (which give rise to optic nerve fibers) in Limulus lateral eyes and their neural coding efficacies were determined over a wide range of light adaptation states and relative stimulus intensities. Extremely stringent data quality procedures were followed to ensure that the results are based on stable preparations. Waveforms which could be compared with those of comparable receptor potentials (RPs) were obtained by constructing plots of the reciprocals of successive interspike intervals, creating instantaneous spike frequency waveforms (ISFWs). Six candidate codes were then measured. They were: the area under the light-evoked ISFW, the mean value of the ISFW, the peak height of the ISFW, the slope of the onset of the ISFW, the duration required for the ISFW to drop from its peak by a given amount, and the duration required for the ISFW to end. Receiver operating characteristic (ROC) analyses were then applied to these coded ISFW values to provide objective indices of AP efficacies in the form of detectability (d') measurements. Several reliable findings were obtained: (1) Both adaptation state and relative intensity affect efficacy. More specifically, the d' values of all codes approach zero, representing chance detectability, when relatively weak flashes are presented in dark-adapted states. (2) Light adaptation produces a sensitivity-acuity tradeoff: as sensitivity decreases in more light-adapted states, detectabilities increase, indicating that ROC-characterized discrimination acuity increases. (3) The AP code efficacy order is similar to but not identical with the efficacy order previously found in photoreceptors: area = peak > or = mean > or = slope = duration-end = duration-drop. The previously measured photoreceptor RP efficacies were quantitatively compared with the present AP data from the optic nerve fiber level, with the following results: (1) All efficacies tend to decline at the more proximal neural level. (2) The decline is code dependent and transmission efficacy falls in this order: peak > area > mean > slope = duration-end = duration-drop. (3) The code which transmits best between photoreceptors and optic nerve fibers (i.e., the peak) differs from the code which has the highest efficacy at the photoreceptor level (i.e., the area); at the more proximal level, these two codes have indistinguishable efficacies. These findings support two conclusions: (1) They further demonstrate that arbitrary characterizations of stimulus-response relationships are very likely to be incomplete. This would be particularly important when, as is often the case in brain research, the mean code alone (i.e., the average firing rate) is used to characterize spike potentials. The present data show that the use of that code would have substantially underestimated detectability had it been used alone. (2) The fact that the code which most completely transmits information between cells is not the code which most completely represents information within a cell leads directly to a possible physiological basis for the existence of multiple neural codes. It particularly leads to the following extension of the Task Dependence Hypothesis of neural coding: Different codes may mediate performance in different behavioral tasks because different codes best serve different neural functions.

Action Potentials↗

PubMed1985

Action potentials in normal and Shaker mutant Drosophila.

Intracellular microelectrode recordings from the cervical giant fiber of normal Drosophila show a characteristic action potential waveform for this identified neuron. The action potential has a rapid initial spike followed by a prominent depolarizing afterpotential. Pharmacological experiments suggest that the giant fiber action potential depends on inward currents carried by Na+ and outward currents carried by K+. Abnormal action potentials are seen in Shaker (Sh) mutant Drosophila. This study compares the effects of six Sh alleles. In each case, abnormalities are limited to action potential repolarization. There are, however, allelic differences. Five alleles cause delayed repolarization and increased action potential durations. Going from most to least extreme, these alleles are: Sh102 greater than ShKS133 greater than ShM greater than ShE62 greater than ShrKO120. Compared to normal action potentials, durations in the extreme mutants are longer by an order of magnitude or more. One mutant allele, Sh5 appears to cause an incompletely repolarized action potential, rather than a repolarization delay.

Action Potentials↗

PubMed1989

Electrodiagnosis of human dorsal sacral nerve roots by recording afferent and efferent extracellular action potentials.

Single extracellular nerve action potentials from afferent fibres with various functions were recorded from human sacral nerve roots. It was shown that the potentials from these fibres can have different wave forms (amplitude, duration) and conduction velocities. The smaller potentials with longer durations have lower cut-off frequencies for certain identification than the larger potentials of shorter duration. The conduction velocity diagnosis covers a range of velocities with a factor of about 10. The slowest measured conduction velocities were between 4 and 10 m/sec. The identification of the functions of afferents in nerve roots is possible by calculating conduction velocities and stimulated activity increase measurements. Besides touch and pain fibres from the skin, afferents from mechano-receptors of the urinary bladder and the anal canal could be detected in dorsal sacral roots. There is evidence of motoneurons in the dorsal sacral roots supplying fatigue resistant muscle fibres. Sacral nerve root electrodiagnosis can be used in operations to identify physiologically-stimulated afferents and reflex activated motoneurons and, therefore, possibly will be useful in nerve anastomoses and nerve root stimulations in paraplegia.

Action Potentials↗

PubMed1982

Two types of scorpion receptor sites, one related to the activation, the other to the inactivation of the action potential sodium channel.

The action of the neurotoxin in Buthinae scorpion venoms (Androctonus, Buthus or Leiurus genera) has been extensively studied. These proteins induce a prolongation of the action potential of nerves and muscles by slowing down inactivation of the sodium channel. Their affinity for their receptor site depends on membrane potential. In the present report we describe a toxin from a Centrurinae scorpion, Centruroides suffusus, which binds rat brain synaptosomes at a receptor site distinct from the Buthinae scorpion site independently of voltage. We name Androctonus-like toxins, alpha-scorpion toxins (alpha-ScTX), and Centruroides-like toxins, beta-scorpion toxins (beta-ScTX). We further report that beta-ScTX induces repetitive firing in frog myelinated nerve fibres by producing an abnormal sodium permeability. The beta-toxin binds specifically to rat brain synaptosomes (Kd = 3 nM) and induces an inhibition of the uptake and a stimulation of the release of GABA at concentrations which are in good agreement with the Kd value. These effects are blocked by tetrodotoxin. The binding site of beta -ScTX is distinct from those of other neurotoxins acting on the sodium channel like tetrodotoxin, alpha-ScTX and veratridine. The alpha-ScTX/beta-ScTX binding site capacities decreases as development of rat brain synaptosomes progresses ; at day 7 after birth, it is 1.1. and at day 39, 0.3.

Action Potentials↗

PubMed2001

[Study on the latency difference between compound muscle and sensory nerve action potentials].

In motor nerve conduction studies compound muscle action potentials (CMAPs) appear later than sensory nerve action potentials (SNAPs). This time lag originates from the conduction delay at the distal motor axon, neuromuscular transmission time and muscle action potential induction time. To investigate the latency difference between CMAPs and SNAPs we studied 46 healthy individuals, 46 patients with diabetes mellitus and 33 patients with carpal tunnel syndrome, using the lumbrical and interossei recording method. In this method the recording active electrode was placed on the 2nd lumbrical muscle and the reference electrode on the proximal palmar aspect of the index finger. Supramaximal stimulation was given to the median or ulnar nerve trunk at 9-cm proximal to the recording active electrode. The CMAP from the 2nd lumbrical muscle (L) and the SNAP from the digital nerve (N) were recorded after median nerve stimulation, and the CMAP from the 2nd interossei muscles (I) was recorded after ulnar nerve stimulation. The residual latency, which is arbitrary defined as the latency difference (L-N) in this study, was 1.38 +/- 0.15 (mean +/- SD) msec in healthy individuals. About 1 msec of the residual latency is regarded as the time for neuromuscular transmission and the time to evoke muscle activities. Thus, the conduction delay at the distal motor axon was calculated as about 0.4 msec in healthy individuals. The residual latency was relatively constant in 29 diabetic patients without conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) < or = 0.4 msec. Their sensory nerve conduction velocities (calculated from N latency) were always above 40 m/sec. On the other hand in diabetic patients with conduction delay across the carpal tunnel, which was defined by the latency difference (L-I) > 0.4 msec, the residual latency gradually increased as the sensory nerve conduction velocity decreased. Their sensory nerve conduction velocities were mostly less than 40 m/sec. The similar relationship was observed in patients with carpal tunnel syndrome without diabetes mellitus. We consider that the diabetic neuropathy alone doesn't cause the increase of the residual latency. Instead, severe conduction delay across the carpal tunnel decreases the N velocity and increases the residual latency. We can also regard the relationship between the latency difference (L-N) and N velocity as being in inverse proportion. Perhaps the increase of the residual latency was simply caused by the proportional decrease in the conduction velocity at the distal motor axon, not by the special mechanism concerning to the carpal tunnel syndrome. This paper presented the electrophysiological changes seen in the distal segment secondary to the proximal entrapment.

Action Potentials↗

PubMed2001

Digit distribution of proper digital nerve action potential.

Antidromic sensory nerve action potential testing is well characterized and commonly used to assess the sensory component of the upper limb median and ulnar nerves. The final terminal segments of these nerves are the proper digital nerves. Ring recording electrodes are commonly used to detect the proper digital nerves' antidromic responses. Attempts to record the separate contributions of individual digital nerves along the lateral aspects of each finger, using small surface electrodes, is shown to be unreliable for determining the integrity of a single terminal digital branch. We found between 50% to 77% of the stimulated terminal branch's response amplitude when recorded at electrodes positioned over the nonstimulated branch located 180 degrees from the activated terminal branch. Detecting a single terminal nerve response was achieved by using the fourth digit and the second digit with one of the second digit's branches neurophysiologically blocked by local anesthetic. The volume-conducted response from the opposite side of the finger resulted in this relatively large recorded response, which remains within the range of reference values precluding the simple use of antidromic techniques to assess injury to a single proper digital nerve. Techniques are proposed to avoid such pitfalls and to assess most accurately the desired response.

Action Potentials↗

PubMed2002

Time-dependent transients in an ionically based mathematical model of the canine atrial action potential.

Ionically based cardiac action potential (AP) models are based on equations with singular Jacobians and display time-dependent AP and ionic changes (transients), which may be due to this mathematical limitation. The present study evaluated transients during long-term simulated activity in a mathematical model of the canine atrial AP. Stimulus current assignment to a specific ionic species contributed to stability. Ionic concentrations were least disturbed with the K(+) stimulus current. All parameters stabilized within 6-7 h. Inward rectifier, Na(+)/Ca(2+) exchanger, L-type Ca(2+), and Na(+)-Cl(-) cotransporter currents made the greatest contributions to stabilization of intracellular [K(+)], [Na(+)], [Ca(2+)], and [Cl(-)], respectively. Time-dependent AP shortening was largely due to the outward shift of Na(+)/Ca(2+) exchange related to intracellular Na(+) (Na) accumulation. AP duration (APD) reached a steady state after approximately 40 min. AP transients also occurred in canine atrial preparations, with the APD decreasing by approximately 10 ms over 35 min, compared with approximately 27 ms in the model. We conclude that model APD and ionic transients stabilize with the appropriate stimulus current assignment and that the mathematical limitation of equation singularity does not preclude meaningful long-term simulations. The model agrees qualitatively with experimental observations, but quantitative discrepancies highlight limitations of long-term model simulations.

Action Potentials↗

PubMed1986

The ionic requirements for the production of action potential in Achatina fulica Ferussac neuron.

The ionic requirement for the production of directly elicited action potentials of a tonically auto-active neuron (TAN) in the subesophageal ganglia of the giant African snail, Achatina fulica Ferussac, was studied electrophysiologically. Calcium free Ringer solution containing 1 mM EDTA reversibly abolished the directly elicited action potential. Verapamil (10 micrograms/ml) or cocaine (4 mg/ml) decreased both amplitude and Vmax of the action potentials. The amplitude of the action potential was also slightly decreased in sodium free choline Ringer. However, tetrodotoxin did not significantly affect either the amplitude or Vmax of the directly elicited action potentials. The results suggest that the ionic requirement for generating action potential in snail neuron is not an ordinary sodium spike. Both calcium and sodium ions may participate in carrying charges across the membrane of the action potential.

Action Potentials↗

PubMed1988

Effect of intravenous ketanserin on the human action potential duration at fixed heart rate.

In this study any changes in action potential duration or Q-T interval due to acute doses of ketanserin were monitored. The effect of a bolus dose (10 or 20 mg) followed by an infusion (10 or 20 mg over 20 minutes) of ketanserin on the Q-T interval and action potential duration was studied in six patients undergoing routine cardiac catheterization. Action potential duration was measured with a silver-silver chloride electrode catheter while heart rate was kept constant by atrial pacing and reflex effects avoided by beta-adrenergic blockade. There were some prolongations of the action potential duration but they were not in excess of 40 msec and did not reach statistical significance (control 263 +/- 46.0 msec; bolus 269 +/- 52.1 msec; infusion 262 +/- 53.6 msec; nor were there any significant changes in Q-T interval. Thus acute intravenous doses of ketanserin, in the absence of hypokalaemia or other Q-T interval-prolonging drugs, have no consistent effect on Q-T interval or action potential duration; prolongation of the action potential, when it occurs, is small.

Action Potentials↗

PubMed1988

Ionic mechanisms underlying action potentials in myometrium.

1. The ionic mechanisms underlying the simple spike action potential in longitudinal myometrium of pregnant rats and the complex action potential which occurs in the same layer of pregnant guinea-pigs are discussed. 2. The current during the upstroke of the simple spike is carried by calcium and repolarization results from inactivation of the calcium current and activation of a potassium current. 3. A slow inward current underlies the plateau component of the complex action potential and calcium is involved in carrying or regulating this current. 4. Single channel recordings from the longitudinal myometrium of pregnant guinea-pigs reveal large conductance (130-170 pS) potassium channels which are activated by depolarization of the membrane. The activation of these channels during the upstroke of the spike would contribute to the rapid termination of the spike. 5. The duration of the plateau component of the complex action potential closely correlates with the duration of contraction and it is suggested that sufficient calcium may enter the cell during the action potential to activate the contractile apparatus directly.

Action Potentials↗

PubMed1996

Unique properties of cardiac action potentials recorded with voltage-sensitive dyes.

INTRODUCTION: Optical mapping with voltage-sensitive dyes has made it possible to record cardiac action potentials with high spatial resolution that is unattainable by conventional techniques. Optically recorded signals possess distinct properties that differ importantly from electrograms recorded with extracellular electrodes or action potentials recorded with microelectrode techniques. Despite the growing application of optical mapping to cardiac electrophysiology, relatively little quantitative information is available regarding the characteristics of optical action potentials recorded from cardiac tissue. METHODS AND RESULTS: A high-resolution optical mapping system and microelectrode techniques were used to determine the characteristics of guinea pig ventricular action potentials recorded with the voltage-sensitive dye di-4-ANEPPS. The effects of optical magnification, tissue-light interaction, sampling rate, voltage resolution, spatial resolution, and cardiac motion on action potential signal characteristics were determined. The optical action potential signal represents the relative change in transmembrane potential arising from a volume of cells, where the area of a recording site is determined by optical magnification and detector area, and the depth of recording is determined by system optics and the visible light transmission characteristics of cardiac muscle. Using photographic lenses, the depth of tissue contributing to the signal is < 250 microns. The action potential plateau and final repolarization can be accurately reconstructed from data digitized at modest sampling rates (450 to 750 Hz), since the frequency content of optical action potentials is band-limited to approximately 150 Hz. However, faster sampling rates are needed to depict the subtle details of the action potential upstroke. In addition to temporal resolution, it is essential to achieve sufficient dynamic range and voltage resolution to accurately represent the time course of membrane potential change. Voltage resolution is inversely related to the square of spatial resolution, hence, there exists an inherent trade-off between increased spatial resolution and diminished voltage resolution. Cardiac motion, which can otherwise limit spatial resolution as well as signal fidelity, can be effectively reduced using mechanical stabilization of the heart without distorting action potential characteristics. CONCLUSIONS: Optical mapping with voltage-sensitive dyes provides high-fidelity multisite action potential recording with flexible spatial resolution. When recording cardiac action potentials with voltage-sensitive dyes, the interdependence of temporal, spatial, and voltage resolutions must be carefully considered.

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