Action Potential Differences Research Articles

Electrophysiological heterogeneity in large populations of rabbit ventricular cardiomyocytes.

Cardiac electrophysiological heterogeneity includes: (i) regional differences in action potential (AP) waveform, (ii) AP waveform differences in cells isolated from a single region, (iii) variability of the contribution of individual ion currents in cells with similar AP durations (APDs). The aim of this study is to assess intra-regional AP waveform differences, to quantify the contribution of specific ion channels to the APD via drug responses and to generate a population of mathematical models to investigate the mechanisms underlying heterogeneity in rabbit ventricular cells. APD in ∼50 isolated cells from subregions of the LV free wall of rabbit hearts were measured using a voltage-sensitive dye. When stimulated at 2 Hz, average APD90 value in cells from the basal epicardial region was 254 ± 25 ms (mean ± standard deviation) in 17 hearts with a mean interquartile range (IQR) of 53 ± 17 ms. Endo-epicardial and apical-basal APD90 differences accounted for ∼10% of the IQR value. Highly variable changes in APD occurred after IK(r) or ICa(L) block that included a sub-population of cells (HR) with an exaggerated (hyper) response to IK(r) inhibition. A set of 4471 AP models matching the experimental APD90 distribution was generated from a larger population of models created by random variation of the maximum conductances (Gmax) of 8 key ion channels/exchangers/pumps. This set reproduced the pattern of cell-specific responses to ICa(L) and IK(r) block, including the HR sub-population. The models exhibited a wide range of Gmax values with constrained relationships linking ICa(L) with IK(r), ICl, INCX, and INaK. Modelling the measured range of inter-cell APDs required a larger range of key Gmax values indicating that ventricular tissue has considerable inter-cell variation in channel/pump/exchanger activity. AP morphology is retained by relationships linking specific ionic conductances. These interrelationships are necessary for stable repolarization despite large inter-cell variation of individual conductances and this explains the variable sensitivity to ion channel block.

Pacsin 2 is required for the maintenance of a normal cardiac function in the developing mouse heart

The Pacsin proteins (Pacsin 1, 2 and 3) play an important role in intracellular trafficking and thereby signal transduction in many cells types. This study was designed to examine the role of Pacsin 2 in cardiac development and function. We investigated the development and electrophysiological properties of Pacsin 2 knockout (P2KO) hearts and single cardiomyocytes isolated from 11.5 and 15.5days old fetal mice. Immunofluorescence experiments confirmed the lack of Pacsin 2 protein expression in P2KO cardiac myocytes in comparison to wildtype (WT). Western blotting demonstrates low expression levels of connexin 43 and T-box 3 proteins in P2KO compared to wildtype (WT). Electrophysiology measurements including online Multi-Electrode Array (MEA) based field potential (FP) recordings on isolated whole heart of P2KO mice showed a prolonged AV-conduction time. Patch clamp measurements of P2KO cardiomyocytes revealed differences in action potential (AP) parameters and decreased pacemaker funny channel (If), as well as L-type Ca2+ channel (ICaL), and sodium channel (INa). These findings demonstrate that Pacsin 2 is necessary for cardiac development and function in mouse embryos, which will enhance our knowledge to better understand the genesis of cardiovascular diseases.

Action potential contour contributes to species differences in repolarization response to β-adrenergic stimulation.

Repolarization response to β-adrenergic (β-AR) stimulation differs between guinea-pig and canine myocytes and, within the latter, between myocardial layers. Correlative analysis suggests that this may be due to differences in action potential (AP) contour. Here we tested whether AP contour may set the response of current and of repolarization to β-AR stimulation (10 nM isoproterenol, ISO). The responses of AP and current to ISO were measured under I-clamp and "AP-clamp" in guinea-pig (GP), dog epicardial (DEPI) and dog subendocardial (DENDO) myocytes. Dynamic-clamp (DC) was used to evaluate the impact of AP features on AP response to ISO. ISO prolonged AP duration (APD) in GP myocytes, did not affect it in DENDO and shortened it in DEPI ones. The current induced by ISO (IISO) sharply differed between GP and canine myocytes and, to a lesser extent, between DENDO and DEPI ones. Differences in IISO profile likely important in setting APD response (time-to-peak, time-to-reversal), were minimized when canine myocytes where clamped with GP AP-waveforms and vice versa. Introduction of a "notch" in GP AP (by DC) was alone insufficient to affect the APD response to ISO; nevertheless, when incorporated in a GP AP-waveform, the main "canine" AP features ("notch" and low plateau potential) caused IISO of GP myocytes to acquire canine features. Early repolarization contour and level of plateau potential contribute to species-specificity of IISO profile. Changes in AP contour, also when generated by modulation of ISO-insensitive currents, may be crucial in setting APD response to β-AR stimulation.

Simultaneous conduction mapping and intracellular membrane potential recording in isolated atria.

We describe a novel approach for simultaneously determining regional differences in action potential (AP) morphology and tissue electrophysiological properties in isolated atria. The epicardial surface of rat atrial preparations was placed in contact with a multi-electrode array (9 × 10 silver chloride electrodes, 0.1 mm diameter and 0.1 mm pitch). A glass microelectrode (100 MΩ) was simultaneously inserted into the endocardial surface to record intracellular AP from either of 2 regions (A, B) during pacing from 2 opposite corners of the tissue. AP duration at 80% of repolarisation and its restitution curve was significantly different only in region A (p < 0.01) when AP was initiated at different stimulation sites. Alternans in AP duration and AP amplitude, and in conduction velocity were observed during 2 separate arrhythmic episodes. This approach of combining microelectrode array and intracellular membrane potential recording may provide new insights into arrhythmogenic mechanisms in animal models of cardiovascular disease.

YIA3 Regional Action Potential Gradients in the Murine Left Atrium

Background Regional differences in action potential (AP) morphology in the adult left atrium (LA) may account for susceptibility to atrial fibrillation. The posterior LA wall close to the junction with the pulmonary veins (LA-PV) is an important area contributing to initiation and maintenance of atrial fibrillation. The posterior LA has a distinct embryologic origin: Its development is regulated by PITX2, a gene that has been inflicted in the genetic predisposition to AF. So far, it is not known whether the electrophysiology of the posterior LA differs from that of other parts of the LA. We therefore characterised the electrical phenotype of the LA-PV compared to other LA regions. Methods Transmembrane (TAPs) and optical (OAPs) action potentials were recorded from 20 superfused murine LA taken from 12 male and 8 female mice aged 12–20 W, bred on an MF1 background. Optical high-density AP mapping was performed and optical APs were recorded from 9 regions across the LA using a dedicated murine activation system (Hamamatsu ORCA flash 4, Di-4-Anepps, sampling rate 1–2 kHz). OAPs were analysed using custom made algorithms produced in MATLAB. At each cycle length, 25 action potentials were averaged to generate a mean waveform that was then used for analysis. TAPs were recorded from 3 LA regions: 1) the posterior LA towards the junction with the pulmonary vein (LA-PV), 2) the medial dome (LA-M) and 3) the LA lateral wall (LA-LW). All Preparations were paced at 100ms. Results OAP distribution maps (n = 8 LA) identified a LA-PV to LA-LW pattern of APD shortening and also demonstrated that there is relatively high local APD heterogeneity within the LA-PV region. TAP recordings identified a higher action potential amplitude (APA) in the LA-PV (84 ± 2 mV) than LA-M (78 ± 1 mV, p Conclusion Regional AP differences in the murine LA clearly suggest that the posterior left atrium has a distinct electrophysiological profile which may render this region susceptible to the genesis and maintenance of AF. Prolonged APD and higher AP amplitude suggest a role as a driver of electrical LA activity. Further studies are warranted to determine whether PITX2 is important for the maintenance of these electrophysiological differences.

Human pluripotent stem cell-derived cardiomyocytes: response to TTX and lidocain reveals strong cell to cell variability.

Stem cell derived cardiomyocytes generated either from human embryonic stem cells (hESC-CMs) or human induced pluripotent stem cells (hiPSC-CMs) hold great promise for the investigation of early developmental processes in human cardiomyogenesis and future cell replacement strategies. We have analyzed electrophysiological properties of hESC-CMs (HES2) and hiPSC-CMs, derived from reprogrammed adult foreskin fibroblasts that have previously been found to be highly similar in terms of gene expression. In contrast to the similarity found in the expression profile we found substantial differences in action potentials (APs) and sodium currents at late stage (day 60) of in vitro differentiation with higher sodium currents in hiPSC-CMs. Sensitivity to lidocain was considerably reduced in hESC-CMs as compared to hiPSC-CMs, and the effect could not be explained by differences in beating frequency. In contrast, sensitivity to tetrodotoxin (TTX) was higher in hESC-CMs suggesting different contributions of TTX-sensitive and TTX-resistant sodium channels to AP generation. These data point to physiological differences that are not necessarily detected by genomics. We conclude that novel pharmacological screening-assays using hiPSC-CMs need to be applied with some caution.

Inherited Cardiac Arrhythmia Syndrome: Role of Potassium Channels

Potassium channels are the main contributors to repolarizing outward currents acting during cardiac action potential. Quantitative and qualitative variations in the expression and biophysical properties of voltage-gated potassium channels seem to be largely responsible for action potential differences observed among regions of the heart and between normal and diseased myocardium. This review discusses the role of potassiumchannel dysfunctions in inherited cardiac arrhythmia syndromes classified as channelopathies caused by either loss-of-function mutations (long QT syndrome [LQTS] and Andersen-Tawil syndrome [ATS]) or gain-of-function mutations in genes encoding potassium channels (short QT syndrome [SQTS] and familial atrial fibrillation [AF]). Early repolarization syndrome and Brugada syndrome are not included in the gain-offunction mutations although they can also be caused by a gain of function in the cardiac KATP Kir 6.1 channel (KCNJ8-S422L) ; they are discussed by Yan and Antzelevitch elsewhere in this issue.

Na+ imaging reveals little difference in action potential–evoked Na+ influx between axon and soma

In cortical pyramidal neurons, the axon initial segment (AIS) is pivotal in synaptic integration. It has been asserted that this is because there is a high density of Na(+) channels in the AIS. However, we found that action potential-associated Na(+) flux, as measured by high-speed fluorescence Na(+) imaging, was about threefold larger in the rat AIS than in the soma. Spike-evoked Na(+) flux in the AIS and the first node of Ranvier was similar and was eightfold lower in basal dendrites. At near-threshold voltages, persistent Na(+) conductance was almost entirely axonal. On a time scale of seconds, passive diffusion, and not pumping, was responsible for maintaining transmembrane Na(+) gradients in thin axons during high-frequency action potential firing. In computer simulations, these data were consistent with the known features of action potential generation in these neurons.

Mechanisms of Transition from Normal to Reentrant Electrical Activity in a Model of Rabbit Atrial Tissue: Interaction of Tissue Heterogeneity and Anisotropy

Experimental evidence suggests that regional differences in action potential (AP) morphology can provide a substrate for initiation and maintenance of reentrant arrhythmias in the right atrium (RA), but the relationships between the complex electrophysiological and anatomical organization of the RA and the genesis of reentry are unclear. In this study, a biophysically detailed three-dimensional computer model of the right atrial tissue was constructed to study the role of tissue heterogeneity and anisotropy in arrhythmogenesis. The model of Lindblad et al. for a rabbit atrial cell was modified to incorporate experimental data on regional differences in several ionic currents (primarily, I Na, I CaL, I K1, I to, and I sus) between the crista terminalis and pectinate muscle cells. The modified model was validated by its ability to reproduce the AP properties measured experimentally. The anatomical model of the rabbit RA (including tissue geometry and fiber orientation) was based on a recent histological reconstruction. Simulations with the resultant electrophysiologically and anatomically detailed three-dimensional model show that complex organization of the RA tissue causes breakdown of regular AP conduction patterns at high pacing rates (>11.75 Hz): as the AP in the crista terminalis cells is longer, and electrotonic coupling transverse to fibers of the crista terminalis is weak, high-frequency pacing at the border between the crista terminalis and pectinate muscles results in a unidirectional conduction block toward the crista terminalis and generation of reentry. Contributions of the tissue heterogeneity and anisotropy to reentry initiation mechanisms are quantified by measuring action potential duration (APD) gradients at the border between the crista terminalis and pectinate muscles: the APD gradients are high in areas where both heterogeneity and anisotropy are high, such that intrinsic APD differences are not diminished by electrotonic interactions. Thus, our detailed computer model reconstructs complex electrical activity in the RA, and provides new insights into the mechanisms of transition from focal atrial tachycardia into reentry.

Mathematical model of the neonatal mouse ventricular action potential

Therapies for heart disease are based largely on our understanding of the adult myocardium. The dramatic differences in action potential (AP) shape between neonatal and adult cardiac myocytes, however, indicate that a different set of molecular interactions in neonatal myocytes necessitates different treatment for newborns. Computational modeling is useful for synthesizing data to determine how interactions between components lead to systems-level behavior, but this technique has not been used extensively to study neonatal heart cell function. We created a mathematical model of the neonatal (day 1) mouse myocyte by modifying, on the basis of experimental data, the densities and/or formulations of ion transport mechanisms in an adult cell model. The new model reproduces the characteristic AP shape of neonatal cells, with a brief plateau phase and longer duration than the adult (action potential duration at 80% repolarization = 60.1 vs. 12.6 ms). The simulation results are consistent with experimental data, including 1) decreased density and altered inactivation of transient outward K+ currents, 2) increased delayed rectifier K+ currents, 3) Ca2+ entry through T-type as well as L-type Ca2+ channels, 4) increased Ca2+ influx through Na+/Ca2+ exchange, and 5) Ca2+ transients resulting from transmembrane Ca2+ entry rather than release from the sarcoplasmic reticulum (SR). Simulations performed with the model generated novel predictions, including increased SR Ca2+ leak and elevated intracellular Na+ concentration in neonatal compared with adult myocytes. This new model can therefore be used for testing hypotheses and obtaining a better quantitative understanding of differences between neonatal and adult physiology.

Differences in striatal spiny neuron action potentials between the spontaneously hypertensive and Wistar-Kyoto rat strains

The spontaneously hypertensive rat (SHR) and the Wistar-Kyoto (WKY) inbred rat strains display behavioral differences characterized by relative increases and decreases in levels of activity. Both strains have subsequently been utilized as animal models of hyperactive and hypoactive behavioral traits. The etiology of these behavioral characteristics is poorly understood, but may stem from alterations in the physiology of selected neural circuits or catecholamine systems. This study investigated the cellular properties of neurons from three genetically related strains: the SHR; WKY; and Wistar (WI). In vivo intracellular recordings were made under urethane anesthesia from spiny projection neurons in the striatum, a brain area involved in behavioral activation. Results obtained from 71 spiny projection neurons indicate that most cellular properties of these neurons were very similar across the three strains. However, the amplitude and half-duration of both spontaneously occurring and current-evoked action potentials were found to be significantly different between the SHR and WKY strains with neurons from the SHR firing action potentials of relatively greater amplitude and shorter duration. Action potential parameters measured from the WI rats were intermediate between the two other strains. These differences in action potentials between two behaviorally distinct strains may reflect altered functioning of particular membrane conductances.

Mechanisms underlying variations in excitation–contraction coupling across the mouse left ventricular free wall

Ca(2+) release during excitation-contraction (EC) coupling varies across the left ventricular free wall. Here, we investigated the mechanisms underlying EC coupling differences between mouse left ventricular epicardial (Epi) and endocardial (Endo) myocytes. We found that diastolic and systolic [Ca(2+)](i) was higher in paced Endo than in Epi myocytes. Our data indicated that differences in action potential (AP) waveform between Epi and Endo cells only partially accounted for differences in [Ca(2+)](i). Rather, we found that the amplitude of the [Ca(2+)](i) transient, but not its trigger - the Ca(2+) current - was larger in Endo than in Epi cells. We also found that spontaneous Ca(2+) spark activity was about 2.8-fold higher in Endo than in Epi cells. Interestingly, ryanodine receptor type 2 (RyR2) protein expression was nearly 2-fold higher in Endo than in Epi myocytes. Finally, we observed less Na(+)-Ca(2+) exchanger function in Endo than in Epi cells, which was associated with decreased Ca(2+) efflux during the AP; this contributed to higher diastolic [Ca(2+)](i) and SR Ca(2+) in Endo than in Epi cells during pacing. We propose that transmural differences in AP waveform, SR Ca(2+) release, and Na(+)-Ca(2+) exchanger function underlie differences in [Ca(2+)](i) and EC coupling across the left ventricular free wall.

Acoustic environment determines phosphorylation state of the Kv3.1 potassium channel in auditory neurons

Sound localization by auditory brainstem nuclei relies on the detection of microsecond interaural differences in action potentials that encode sound volume and timing. Neurons in these nuclei express high amounts of the Kv3.1 potassium channel, which allows them to fire at high frequencies with short-duration action potentials. Using computational modeling, we show that high amounts of Kv3.1 current decrease the timing accuracy of action potentials but enable neurons to follow high-frequency stimuli. The Kv3.1b channel is regulated by protein kinase C (PKC), which decreases current amplitude. Here we show that in a quiet environment, Kv3.1b is basally phosphorylated in rat brainstem neurons but is rapidly dephosphorylated in response to high-frequency auditory or synaptic stimulation. Dephosphorylation of the channel produced an increase in Kv3.1 current, facilitating high-frequency spiking. Our results indicate that the intrinsic electrical properties of auditory neurons are rapidly modified to adjust to the ambient acoustic environment.

Differences in action potential and early afterdepolarization properties in LQT2 and LQT3 models of long QT syndrome.

1. Long OT syndrome has many causes from both acquired and congenital disorders. For the congenital disorders, their presentation and disease course are not identical. We studied two pharmacological models of long QT syndrome (LQT) to identify differences in cellular electrophysiological properties that may account for this. LQT2 was simulated by suppression of the rapidly activating delayed rectifier potassium current (I(Kr)) with the drug E-4031, and LQT3 was simulated by slowing of the sodium current (I(Na)) decay with the toxin ATX II. 2. Single rabbit ventricular cell action potentials were studied using the amphotericin B perforated patch clamp technique. Action potential and early afterdepolarization (EAD) properties were rigorously defined by the frequency power spectra obtained with fast Fourier transforms. 3. The E-4031 (n=43 myocytes) and ATX II (n=50 myocytes) models produced different effects on action potential and EAD properties. The major differences are that ATX II, compared with E-4031, caused greater action potential prolongation, more positive plateau voltages, lower amplitude EADs with less negative take-off potentials, greater time to the EAD peak voltage, and longer duration EADs. Despite causing greater action potential prolongation, the incidence of EAD induction was much less with the ATX II model (28%) than with the E-4031 model (84%). Thus these two pharmacological models have strikingly different cellular electrophysiological properties. 4. Our findings provide cellular mechanisms that may account for some differences in the clinical presentation of LQT2 and LQT3.

Differing action potential shapes in rat dorsal root ganglion neurones related to their substance P and calcitonin gene-related peptide immunoreactivity

Intracellular electrophysiological recordings were made in vitro at 36.5 degrees C from lumbar (L4 to L6) dorsal root ganglion neurones of 6-8-week-old female rats. Electrophysiological properties were recorded prior to intracellular injection with fluorescent dye. The following showed substance P-like immunoreactivity (SP-LI): 8/19 C-fibre cells, 6/26 Adelta cells, and 0/52 Aalpha/beta cells. In C-fibre neurones, there were no significant differences in action potential (AP) characteristics between those with SP-LI and those without. In contrast, the Adelta neurones with SP-LI had significantly deeper and longer afterhyperpolarisations (AHPs), but their AP durations did not differ from those without SP-LI. Both SP-LI and calcitonin gene-related peptide-LI (CGRP-LI) were examined on 18 Adelta and 11 C cells. Most (7/8) neurones with SP-LI also showed CGRP-LI, but only 7/21 neurones without SP-LI showed CGRP-LI. One C cell showed SP-LI but no CGRP-LI. Neurones with neither peptide (-/-), with only CGRP (-/CGRP) or with both peptides (SP/CGRP) were compared (n = 28). The numbers in each group were, respectively, 5, 2, and 3 with C-fibres and 9, 5, and 4 with Adelta-fibres. The peptide content and AP shape were related in Adelta neurones. Most -/- Adelta neurones had short APs and short AHPs; most -/CGRP neurones had long APs and long AHPs, and SP/CGRP neurones had short APs with deep, long AHPs. There was a positive correlation between log10 of the area under the AP (AP area) and log10 AHP duration in Adelta neurones. All SP- and most CGRP-containing Adelta neurones had AP shapes similar to those previously described for nociceptive neurones. However, a few without peptide also showed such properties, raising the possibility that some nociceptive neurones did not express these peptides.

Developmental changes in Na+ conductances in rat neocortical neurons: appearance of a slowly inactivating component

1. Na+ conductances have been characterized in rat neocortical neurons from the sensorimotor area. Neurons were obtained by acute dissociation from animals at developmental stages from embryonic day 16 (E16) to postnatal day 50 (P50) to quantify any developmental changes in the kinetic properties of the Na+ conductance. 2. Neurons were divided into two classes, based on morphology, to determine whether there are any cell-type specific differences in Na+ conductances that contribute to the different action potential morphologies seen in current-clamp recordings in vitro. 3. Upon isolation, neurons were voltage clamped using the whole-cell variation of the patch-clamp technology. Both cell types, pyramidal and nonpyramidal, demonstrate large increases in Na+ current density during this developmental period (E16-P50). Normalized conductances were near 10 pS/micron2 in neurons from embryonic animals, and increased 6- to 10-fold during the first 2 wk postnatal. The final conductance reached in pyramidal neurons was higher than in non-pyramidal neurons. 4. We found no differences between the two cell types, pyramidal and nonpyramidal, in the voltage dependence of activation, inactivation kinetics, voltage dependence of steady-state inactivation, and recovery from inactivation. 5. The time course of Na+ current in immature neurons were fit with classical Hodgkin-Huxley kinetics. However, in more mature neurons the kinetics of inactivation became more complicated such that two decay components were required to obtain good fit. The slowly decaying component had a time course 5 to 10 times slower than the fast component. 6. Several procedures were used to reduce the magnitude of Na+ conductance in mature neurons to ensure graded, voltage-dependent inward currents. These included reduced extracellular [Na+], submaximal tetrodotoxin concentrations, and reduced holding potential. Under each of these conditions we were able to verify the observation that Na+ current inactivation occurs with two exponentials. 7. Single-channel Na+ currents were obtained from cell-attached patches. The membrane density of active Na+ channels increases with development, and ensemble averages from mature neurons demonstrated two inactivation processes. The slow inactivation process was accounted for by long-latency single-channel openings of the same amplitude as the short-latency openings. 8. We conclude that there are no kinetic differences in the Na+ channels between cell types. Differences in action potentials are then not explained by differences in Na+ current kinetics, but might be partially explained by the different densities.(ABSTRACT TRUNCATED AT 400 WORDS)

Contributions of cellular electrophysiology to the understanding of the electrocardiogram

The understanding of cardiac action potential and membrane currents has broadened the theoretical foundation and enhanced the clinical usefulness of the electrocardiogram. An improved understanding of the morphology of the electrocardiographic waveform has resulted from: correlations between Vmax of depolarization and QRS complex, plateau of the ventricular action potential and S-T segment, terminal repolarization and T-wave, from definitions of action potential differences responsible for the T-wave, and recordings of action potential alternans. Cellular electrophysiology has contributed to the understanding of certain mechanisms of cardiac standstill. Many disturbances of conduction and refractoriness associated with ventricular arrhythmias can be attributed to the following derangements at the cellular level: slowing of terminal repolarization, development of diastolic depolarization in fibers with stable resting membrane potential, after-depolarizations, currents of injury resulting from non-uniform polarization, increased dispersion of action potential durations, and co-existence of slow conduction and short premature action potentials.

Differences in action potentials and accommodation of sensory and motor myelinated nerve fibres as computed on the basis of voltage clamp data.

1. Voltage clamp experiments were performed on sensory and motor nerve fibres of the frog using a digital computer for automatic experiment control and data recording. 2. Rates of rise and maximum amplitudes of potassium currents were determined in both sensory and motor fibres, so that comparative values of n infinity and tau-n could be obtained. 3. The results indicate that the n infinity-V curve for sensory fibres is displaced from the curve for motor fibres in a depolarising direction. The potassium kinetics are similar in both for voltage steps up to about - 20 m V, beyond which tau-n becomes progressively smaller for sensory than for motor fibres. 4. These comparative values of n affinity and tau-n have been used to calculate alpha-n and beta-n values for a model "motor" action potential by considering the Frankenhaeuser-Huxley computed action potential to be "sensory". This modification of the potassium system, together with some alteration to the sodium inactivation system produces a satisfactory model "motor" action potential. 5. The model sensory and motor action potentials behave quite similarly to their experimentally recorded counterparts with respect to action potential shape and relative duration, repetitive firing, accomodation and the simulated action of T.E.A.

Ionic Relations of Cells of Chara Australis V. The Action Potential

The effect of various ions on the resting and action potential differences in single cells of the alga Ohara australis was studied. When the concentration of calcium ions in the external medium was changed by replacement with magnesium ions, keeping the total concentration constant, the peak level of the action potential changed reversibly. The change was about +29 mV per tenfold increase in calcium concentration, over a restricted range of the latter.