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1
Pan, Michael, Peter J. Gawthrop, Kenneth Tran, Joseph Cursons, and Edmund J. Crampin. "Bond graph modelling of the cardiac action potential: implications for drift and non-unique steady states." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 474, no. 2214 (2018): 20180106. http://dx.doi.org/10.1098/rspa.2018.0106.
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Mathematical models of cardiac action potentials have become increasingly important in the study of heart disease and pharmacology, but concerns linger over their robustness during long periods of simulation, in particular due to issues such as model drift and non-unique steady states. Previous studies have linked these to violation of conservation laws, but only explored those issues with respect to charge conservation in specific models. Here, we propose a general and systematic method of identifying conservation laws hidden in models of cardiac electrophysiology by using bond graphs, and develop a bond graph model of the cardiac action potential to study long-term behaviour. Bond graphs provide an explicit energy-based framework for modelling physical systems, which makes them well suited for examining conservation within electrophysiological models. We find that the charge conservation laws derived in previous studies are examples of the more general concept of a ‘conserved moiety’. Conserved moieties explain model drift and non-unique steady states, generalizing the results from previous studies. The bond graph approach provides a rigorous method to check for drift and non-unique steady states in a wide range of cardiac action potential models, and can be extended to examine behaviours of other excitable systems.
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Gaur, Namit, Xiao-Yan Qi, David Benoist, et al. "A computational model of pig ventricular cardiomyocyte electrophysiology and calcium handling: Translation from pig to human electrophysiology." PLOS Computational Biology 17, no. 6 (2021): e1009137. http://dx.doi.org/10.1371/journal.pcbi.1009137.
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The pig is commonly used as an experimental model of human heart disease, including for the study of mechanisms of arrhythmia. However, there exist differences between human and porcine cellular electrophysiology: The pig action potential (AP) has a deeper phase-1 notch, a longer duration at 50% repolarization, and higher plateau potentials than human. Ionic differences underlying the AP include larger rapid delayed-rectifier and smaller inward-rectifier K+-currents (IKr and IK1 respectively) in humans. AP steady-state rate-dependence and restitution is steeper in pigs. Porcine Ca2+ transients can have two components, unlike human. Although a reliable computational model for human ventricular myocytes exists, one for pigs is lacking. This hampers translation from results obtained in pigs to human myocardium. Here, we developed a computational model of the pig ventricular cardiomyocyte AP using experimental datasets of the relevant ionic currents, Ca2+-handling, AP shape, AP duration restitution, and inducibility of triggered activity and alternans. To properly capture porcine Ca2+ transients, we introduced a two-step process with a faster release in the t-tubular region, followed by a slower diffusion-induced release from a non t-tubular subcellular region. The pig model behavior was compared with that of a human ventricular cardiomyocyte (O’Hara-Rudy) model. The pig, but not the human model, developed early afterdepolarizations (EADs) under block of IK1, while IKr block led to EADs in the human but not in the pig model. At fast rates (pacing cycle length = 400 ms), the human cell model was more susceptible to spontaneous Ca2+ release-mediated delayed afterdepolarizations (DADs) and triggered activity than pig. Fast pacing led to alternans in human but not pig. Developing species-specific models incorporating electrophysiology and Ca2+-handling provides a tool to aid translating antiarrhythmic and arrhythmogenic assessment from the bench to the clinic.
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Lei, Chon Lok, Sanmitra Ghosh, Dominic G. Whittaker, et al. "Considering discrepancy when calibrating a mechanistic electrophysiology model." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 378, no. 2173 (2020): 20190349. http://dx.doi.org/10.1098/rsta.2019.0349.
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Uncertainty quantification (UQ) is a vital step in using mathematical models and simulations to take decisions. The field of cardiac simulation has begun to explore and adopt UQ methods to characterize uncertainty in model inputs and how that propagates through to outputs or predictions; examples of this can be seen in the papers of this issue. In this review and perspective piece, we draw attention to an important and under-addressed source of uncertainty in our predictions—that of uncertainty in the model structure or the equations themselves. The difference between imperfect models and reality is termed model discrepancy , and we are often uncertain as to the size and consequences of this discrepancy. Here, we provide two examples of the consequences of discrepancy when calibrating models at the ion channel and action potential scales. Furthermore, we attempt to account for this discrepancy when calibrating and validating an ion channel model using different methods, based on modelling the discrepancy using Gaussian processes and autoregressive-moving-average models, then highlight the advantages and shortcomings of each approach. Finally, suggestions and lines of enquiry for future work are provided. This article is part of the theme issue ‘Uncertainty quantification in cardiac and cardiovascular modelling and simulation’.
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O'Hara, Thomas, and Yoram Rudy. "Quantitative comparison of cardiac ventricular myocyte electrophysiology and response to drugs in human and nonhuman species." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 5 (2012): H1023—H1030. http://dx.doi.org/10.1152/ajpheart.00785.2011.
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Explanations for arrhythmia mechanisms at the cellular level are usually based on experiments in nonhuman myocytes. However, subtle electrophysiological differences between species may lead to different rhythmic or arrhythmic cellular behaviors and drug response given the nonlinear and highly interactive cellular system. Using detailed and quantitatively accurate mathematical models for human, dog, and guinea pig ventricular action potentials (APs), we simulated and compared cell electrophysiology mechanisms and response to drugs. Under basal conditions (absence of β-adrenergic stimulation), Na+/K+-ATPase changes secondary to Na+ accumulation determined AP rate dependence for human and dog but not for guinea pig where slow delayed rectifier current ( IKs) was the major rate-dependent current. AP prolongation with reduction of rapid delayed rectifier current ( IKr) and IKs (due to mutations or drugs) showed strong species dependence in simulations, as in experiments. For humans, AP prolongation was 80% following IKr block. It was 30% for dog and 20% for guinea pig. Under basal conditions, IKs block was of no consequence for human and dog, but for guinea pig, AP prolongation after IKs block was severe. However, with β-adrenergic stimulation, IKs played an important role in all species, particularly in AP shortening at fast rate. Quantitative comparison of AP repolarization, rate-dependence mechanisms, and drug response in human, dog, and guinea pig revealed major species differences (e.g., susceptibility to arrhythmogenic early afterdepolarizations). Extrapolation from animal to human electrophysiology and drug response requires great caution.
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Crampin, Edmund J., Nicolas P. Smith, A. Elise Langham, Richard H. Clayton, and Clive H. Orchard. "Acidosis in models of cardiac ventricular myocytes." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 364, no. 1842 (2006): 1171–86. http://dx.doi.org/10.1098/rsta.2006.1763.
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The effects of acidosis on cardiac electrophysiology and excitation–contraction coupling have been studied extensively. Acidosis decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function. In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different effects to altered Ca 2+ transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to simulate respiratory acidosis in the heart.
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Fink, Martin, Wayne R. Giles, and Denis Noble. "Contributions of inwardly rectifying K + currents to repolarization assessed using mathematical models of human ventricular myocytes." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 364, no. 1842 (2006): 1207–22. http://dx.doi.org/10.1098/rsta.2006.1765.
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Repolarization of the action potential (AP) in cardiac muscle is a major determinant of refractoriness and excitability, and can also strongly modulate excitation–contraction coupling. In clinical cardiac electrophysiology, the Q-T interval, and hence action potential duration, is both an essential marker of normal function and an indicator of risk for arrhythmic events. It is now well known that the termination of the plateau phase of the AP and the repolarization waveform involve a complex interaction of transmembrane ionic currents. These include a slowly inactivating Na + current, inactivating Ca 2+ current, the decline of an electrogenic current due to Na + /Ca 2+ exchange and activation of three or four different K + currents. At present, many of the quantitative aspects of this important physiological and pathophysiological process remain incompletely understood. Recently, three mathematical models of the membrane AP in human ventricle myocyte have been developed and made available on the Internet. In this study, we have implemented these models for the purpose of comparing the K + currents, which are responsible for terminating the plateau phase of the AP and generating its repolarization. In this paper, our emphasis is on the two highly nonlinear inwardly rectifying potassium currents, and . A more general goal is to obtain improved understanding of the ionic mechanisms, which underlie all-or-none repolarization and the parameter denoted ‘repolarization reserve’ in the human ventricle. Further, insights into these fundamental variables can be expected to provide a more rational basis for clinical assessment of the Q-T and Q-T C intervals, and hence provide insights into some of the very substantial efforts in safety pharmacology, which are based on these parameters.
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Abramson, David, Miguel O. Bernabeu, Blair Bethwaite, et al. "High-throughput cardiac science on the Grid." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1925 (2010): 3907–23. http://dx.doi.org/10.1098/rsta.2010.0170.
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Cardiac electrophysiology is a mature discipline, with the first model of a cardiac cell action potential having been developed in 1962. Current models range from single ion channels, through very complex models of individual cardiac cells, to geometrically and anatomically detailed models of the electrical activity in whole ventricles. A critical issue for model developers is how to choose parameters that allow the model to faithfully reproduce observed physiological effects without over-fitting. In this paper, we discuss the use of a parametric modelling toolkit, called N imrod , that makes it possible both to explore model behaviour as parameters are changed and also to tune parameters by optimizing model output. Importantly, N imrod leverages computers on the Grid, accelerating experiments by using available high-performance platforms. We illustrate the use of N imrod with two case studies, one at the cardiac tissue level and one at the cellular level.
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Tazmini, Kiarash, Michael Frisk, Alexandre Lewalle, et al. "Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes." Circulation Research 126, no. 7 (2020): 889–906. http://dx.doi.org/10.1161/circresaha.119.315641.
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Rationale: Hypokalemia occurs in up to 20% of hospitalized patients and is associated with increased incidence of ventricular and atrial fibrillation. It is unclear whether these differing types of arrhythmia result from direct and perhaps distinct effects of hypokalemia on cardiomyocytes. Objective: To investigate proarrhythmic mechanisms of hypokalemia in ventricular and atrial myocytes. Methods and Results: Experiments were performed in isolated rat myocytes exposed to simulated hypokalemia conditions (reduction of extracellular [K + ] from 5.0 to 2.7 mmol/L) and supported by mathematical modeling studies. Ventricular cells subjected to hypokalemia exhibited Ca 2+ overload and increased generation of both spontaneous Ca 2+ waves and delayed afterdepolarizations. However, similar Ca 2+ -dependent spontaneous activity during hypokalemia was only observed in a minority of atrial cells that were observed to contain t-tubules. This effect was attributed to close functional pairing of the Na + -K + ATPase and Na + -Ca 2+ exchanger proteins within these structures, as reduction in Na + pump activity locally inhibited Ca 2+ extrusion. Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepolarizations during hypokalemia, associated with Ca 2+ overload. However, early afterdepolarizations also occurred in untubulated atrial cells, despite Ca 2+ quiescence. These phase-3 early afterdepolarizations were rather linked to reactivation of nonequilibrium Na + current, as they were rapidly blocked by tetrodotoxin. Na + current-driven early afterdepolarizations in untubulated atrial cells were enabled by membrane hyperpolarization during hypokalemia and short action potential configurations. Brief action potentials were in turn maintained by ultra-rapid K + current (I Kur ); a current which was found to be absent in tubulated atrial myocytes and ventricular myocytes. Conclusions: Distinct mechanisms underlie hypokalemia-induced arrhythmia in the ventricle and atrium but also vary between atrial myocytes depending on subcellular structure and electrophysiology.
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Seemann, Gunnar, Christine Höper, Frank B. Sachse, Olaf Dössel, Arun V. Holden, and Henggui Zhang. "Heterogeneous three-dimensional anatomical and electrophysiological model of human atria." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 364, no. 1843 (2006): 1465–81. http://dx.doi.org/10.1098/rsta.2006.1781.
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Investigating the mechanisms underlying the genesis and conduction of electrical excitation in the atria at physiological and pathological states is of great importance. To provide knowledge concerning the mechanisms of excitation, we constructed a biophysical detailed and anatomically accurate computer model of human atria that incorporates both structural and electrophysiological heterogeneities. The three-dimensional geometry was extracted from the visible female dataset. The sinoatrial node (SAN) and atrium, including crista terminalis (CT), pectinate muscles (PM), appendages (APG) and Bachmann's bundle (BB) were segmented in this work. Fibre orientation in CT, PM and BB was set to local longitudinal direction. Descriptions for all used cell types were based on modifications of the Courtemanche et al . model of a human atrial cell. Maximum conductances of , and were modified for PM, CT, APG and atrioventricular ring to reproduce measured action potentials (AP). Pacemaker activity in the human SAN was reproduced by removing , but including , , and gradients of channel conductances as described in previous studies for heterogeneous rabbit SAN. Anisotropic conduction was computed with a monodomain model using the finite element method. The transversal to longitudinal ratio of conductivity for PM, CT and BB was 1 : 9. Atrial working myocardium (AWM) was set to be isotropic. Simulation of atrial electrophysiology showed initiation of APs in the SAN centre. The excitation spread afterwards to the periphery near to the region of the CT and preferentially towards the atrioventricular region. The excitation extends over the right atrium along PM. Both CT and PM activated the right AWM. Earliest activation of the left atrium was through BB and excitation spread over to the APG. The conduction velocities were 0.6 m s −1 for AWM, 1.2 m s −1 for CT, 1.6 m s −1 for PM and 1.1 m s −1 for BB at a rate of 63 bpm. The simulations revealed that bundles form dominant pathways for atrial conduction. The preferential conduction towards CT and along PM is comparable with clinical mapping. Repolarization is more homogeneous than excitation due to the heterogeneous distribution of electrophysiological properties and hence the action potential duration.
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Roome, Chris J., Emmet M. Power, and Ruth M. Empson. "Transient reversal of the sodium/calcium exchanger boosts presynaptic calcium and synaptic transmission at a cerebellar synapse." Journal of Neurophysiology 109, no. 6 (2013): 1669–80. http://dx.doi.org/10.1152/jn.00854.2012.
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The sodium/calcium exchanger (NCX) is a widespread transporter that exchanges sodium and calcium ions across excitable membranes. Normally, NCX mainly operates in its “forward” mode, harnessing the electrochemical gradient of sodium ions to expel calcium. During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Such “reverse”-mode NCX operation is frequently implicated during pathological or artificially extended periods of depolarization, not during normal activity. We have used fast calcium imaging, mathematical simulation, and whole cell electrophysiology to study the role of NCX at the parallel fiber-to-Purkinje neuron synapse in the mouse cerebellum. We show that nontraditional, reverse-mode NCX activity boosts the amplitude and duration of parallel fiber calcium transients during short bursts of high-frequency action potentials typical of their behavior in vivo. Simulations, supported by experimental manipulations, showed that accumulation of intracellular sodium drove NCX into reverse mode. This mechanism fueled additional calcium influx into the parallel fibers that promoted synaptic transmission to Purkinje neurons for up to 400 ms after the burst. Thus we provide the first functional demonstration of transient and fast NCX-mediated calcium entry at a major central synapse. This unexpected contribution from reverse-mode NCX appears critical for shaping presynaptic calcium dynamics and transiently boosting synaptic transmission, and is likely to optimize the accuracy of cerebellar information transfer.
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Severi, Stefano, Cristiana Corsi, and Elisabetta Cerbai. "From in vivo plasma composition to in vitro cardiac electrophysiology and in silico virtual heart: the extracellular calcium enigma." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 367, no. 1896 (2009): 2203–23. http://dx.doi.org/10.1098/rsta.2009.0032.
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In spite of its potential impact on simulation results, the problem of setting the appropriate Ca 2+ concentration ([Ca 2+ ] o ) in computational cardiac models has not yet been properly considered. Usually [Ca 2+ ] o values are derived from in vitro electrophysiology. Unfortunately, [Ca 2+ ] o in the experiments is set significantly far (1.8 or 2 mM) from the physiological [Ca 2+ ] in blood (1.0–1.3 mM). We analysed the inconsistency of [Ca 2+ ] o among in vivo , in vitro and in silico studies and the dependence of cardiac action potential (AP) duration (APD) on [Ca 2+ ] o . Laboratory measurements confirmed the difference between standard extracellular solutions and normal blood [Ca 2+ ]. Experimental data on human atrial cardiomyocytes confirmed literature data, demonstrating an inverse relationship between APD and [Ca 2+ ] o . Sensitivity analysis of APD on [Ca 2+ ] o for five of the most used cardiac cell models was performed. Most of the models responded with AP prolongation to increases in [Ca 2+ ] o , i.e. opposite to the AP shortening observed in vitro and in vivo. Modifications to the Ten Tusscher–Panfilov model were implemented to demonstrate that qualitative consistency among in vivo , in vitro and in silico studies can be achieved. The Courtemanche atrial model was used to test the effect of changing [Ca 2+ ] o on quantitative predictions about the effect of K + current blockade. The present analysis suggests that (i) [Ca 2+ ] o in cardiac AP models should be changed from 1.8 to 2 mM to approximately 1.15 mM in order to reproduce in vivo conditions, (ii) the sensitivity to [Ca 2+ ] o of ventricular AP models should be improved in order to simulate real conditions, (iii) modifications to the formulation of Ca 2+ -dependent I CaL inactivation can make models more suitable to analyse AP when [Ca 2+ ] o is set to lower physiological values, and (iv) it could be misleading to use non-physiological high [Ca 2+ ] o when the quantitative analysis of in vivo pathophysiological mechanisms is the ultimate aim of simulation.
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Volkov, Alexander G., Daniel J. Collins, and John Mwesigwa. "Plant electrophysiology: pentachlorophenol induces fast action potentials in soybean." Plant Science 153, no. 2 (2000): 185–90. http://dx.doi.org/10.1016/s0168-9452(99)00271-x.
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McBurney, R. N., and S. J. Kehl. "Electrophysiology of neurosecretory cells from the pituitary intermediate lobe." Journal of Experimental Biology 139, no. 1 (1988): 317–28. http://dx.doi.org/10.1242/jeb.139.1.317.
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One of the goals in studying the electrical properties of neurosecretory cells is to relate their electrical activity to the process of secretion. A central question in these studies concerns the role of transmembrane calcium ion flux in the initiation of the secretory event. With regard to the secretory process in pituitary cells, several research groups have addressed this question in vitro using mixed primary anterior pituitary cell cultures or clonal cell lines derived from pituitary tumours. Other workers, including ourselves, have used homogeneous cell cultures derived from the pituitary intermediate lobes of rats to examine the characteristics of voltage-dependent conductances, the contribution of these conductances to action potentials and their role in stimulus-secretion coupling. Pars intermedia (PI) cells often fire spontaneous action potentials whose frequency can be modified by the injection of sustained currents through the recording electrode. In quiescent cells action potentials can also be evoked by the injection of depolarizing current stimuli. At around 20 degrees C these action potentials have a duration of about 5 ms. Although most of the inward current during action potentials is carried by sodium ions, a calcium ion component can be demonstrated under abnormal conditions. Voltage-clamp experiments have revealed that the membrane of these cells contains high-threshold, L-type, Ca2+ channels and low-threshold Ca2+ channels. Since hormone release from PI cells appears not to be dependent on action potential activity but does depend on external calcium ions, it is not clear what role these Ca2+ channels play in stimulus-secretion coupling in cells of the pituitary pars intermedia. One possibility is that the low-threshold Ca2+ channels are more important to the secretory process than the high-threshold channels.
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Huizinga, Jan D. "Action potentials in gastrointestinal smooth muscle." Canadian Journal of Physiology and Pharmacology 69, no. 8 (1991): 1133–42. http://dx.doi.org/10.1139/y91-166.
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Recent investigation of the ultrastracture and electrophysiology of gastrointestinal smooth muscle layers has revealed a fascinating heterogeneity in cell type, cell structure, intercellular communication, and generated electrical activities. Networks of interstitial cells of Cajal (ICC) have been identified in many muscle layers and evidence is accumulating for a role of these networks in gut pacemaking activity. Synchronized motility in the organs of the gut result from interaction between ICC, neural-tissue, and smooth muscle cells. Regulation of cell to cell communication between the different cell types will be an important area for further research. Progress has been made in the elucidation of the ionic basis of the slow wave type action potentials and the spike-like action potentials. The mechanism underlying smooth muscle autorhythmicity seems different from that encountered in cardiac tissue, and evidence exists for metabolic regulation of the frequency of slow wave type action potentials.Key words: pacemaker activity, slow wave, autorhythmicity, interstitial cells of Cajal.
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Li, Xiang, Ji-qian Zhang, and Jian-wei Shuai. "Isoprenaline: A Potential Contributor in Sick Sinus Syndrome—Insights from a Mathematical Model of the Rabbit Sinoatrial Node." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/540496.
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The mechanism of isoprenaline exerting its effects on cardiac pacemaking and driving in sick sinus syndrome is controversial and unresolved. In this paper, mathematical models for rabbit sinoatrial node cells were modified by incorporating equations for the known dose-dependent actions of isoprenaline on various ionic channel currents, the intracellular Ca2+transient, andiNachanges induced by SCN5A gene mutations; the cell models were also incorporated into an intact SAN-atrium model of the rabbit heart that is based on both heterogeneities of the SAN electrophysiology and histological structure. Our results show that, in both central and peripheral cell models, isoprenaline could not only shorten the action potential duration, but also increase the amplitude of action potential. The mutation impaired the SAN pacemaking. Simulated vagal nerve activity amplified the bradycardic effects of the mutation. However, in tissue case, the pacemaker activity may show temporal, spatial, or even spatiotemporal cessation caused by the mutation. Addition of isoprenaline could significantly diminish the bradycardic effect of the mutation and the SAN could restart pacing and driving the surrounding tissue. Positive effects of isoprenaline may primarily be attributable to an increase iniNaandiCa,Twhich were reduced by the mutation.
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Shvetsova, Tatiana, John Mwesigwa, and Alexander G. Volkov. "Plant electrophysiology: FCCP induces action potentials and excitation waves in soybean." Plant Science 161, no. 5 (2001): 901–9. http://dx.doi.org/10.1016/s0168-9452(01)00484-8.
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Manchanda, Rohit, Shailesh Appukuttan, and Mithun Padmakumar. "Electrophysiology of Syncytial Smooth Muscle." Journal of Experimental Neuroscience 13 (January 2019): 117906951882191. http://dx.doi.org/10.1177/1179069518821917.
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As in other excitable tissues, two classes of electrical signals are of fundamental importance to the functioning of smooth muscles: junction potentials, which arise from neurotransmission and represent the initiation of excitation (or in some instances inhibition) of the tissue, and spikes or action potentials, which represent the accomplishment of excitation and lead on to contractile activity. Unlike the case in skeletal muscle and in neurons, junction potentials and spikes in smooth muscle have been poorly understood in relation to the electrical properties of the tissue and in terms of their spatiotemporal spread within it. This owes principally to the experimental difficulties involved in making precise electrical recordings from smooth muscles and also to two inherent features of this class of muscle, ie, the syncytial organization of its cells and the distributed innervation they receive, which renders their biophysical analysis problematic. In this review, we outline the development of hypotheses and knowledge on junction potentials and spikes in syncytial smooth muscle, showing how our concepts have frequently undergone radical changes and how recent developments hold promise in unraveling some of the many puzzles that remain. We focus especially on computational models and signal analysis approaches. We take as illustrative examples the smooth muscles of two organs with distinct functional characteristics, the vas deferens and urinary bladder, while also touching on features of electrical functioning in the smooth muscles of other organs.
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Klabunde, Richard E. "Cardiac electrophysiology: normal and ischemic ionic currents and the ECG." Advances in Physiology Education 41, no. 1 (2017): 29–37. http://dx.doi.org/10.1152/advan.00105.2016.
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Basic cardiac electrophysiology is foundational to understanding normal cardiac function in terms of rate and rhythm and initiation of cardiac muscle contraction. The primary clinical tool for assessing cardiac electrical events is the electrocardiogram (ECG), which provides global and regional information on rate, rhythm, and electrical conduction as well as changes in electrical activity associated with cardiac disease, particularly ischemic heart disease. This teaching review is written at a level appropriate for first- and second-year medical students. Specific concepts discussed include ion equilibrium potentials, electrochemical forces driving ion movements across membranes, the role of ion channels in determining membrane resting potentials and action potentials, and the conduction of action potentials within the heart. The electrophysiological basis for the ECG is then described, followed by discussion on how ischemia alters cellular electrophysiology and ECG recordings, with particular emphasis on changes in T waves and ST segments of the ECG.
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Hewett, K. W., C. H. Gaymes, C. I. Noh, et al. "Cellular electrophysiology of neonatal and adult rabbit atrioventricular node." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (1991): H1674—H1684. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1674.
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Adult and neonatal rabbit atrioventricular node (AVN) preparations were studied using transmembrane and surface electrogram recordings. Action potentials were categorized into four types, atrionodal (AN), nodal (N), “high” nodo-His (NH) (HNH), and “low” NH (LNH), according to their action potential characteristics and their location within the A-H interval. The electrophysiological parameters of the lower three regions were identical between the two age groups. Action potentials from the neonatal AN region were lower in amplitude and maximum diastolic potential than they were in the adult. The N cell action potential parameters did not differ between the two age groups, however, there did appear to be qualitative differences. AVN conduction times (A-H intervals) were the same in both age groups, as were the antegrade and retrograde refractory periods, and the Wenckebach intervals. Pacemaker activity was significantly greater in the neonates than in the adults and, in 11 of 13 neonatal preparations, originated in the AN region or higher. In 13 of 14 adult preparations, pacemaker activity resided within the AVN.
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Rudy, Yoram, and Jonathan R. Silva. "Computational biology in the study of cardiac ion channels and cell electrophysiology." Quarterly Reviews of Biophysics 39, no. 1 (2006): 57–116. http://dx.doi.org/10.1017/s0033583506004227.
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1. Prologue 582. The Hodgkin–Huxley formalism for computing the action potential 592.1 The axon action potential model 592.2 Cardiac action potential models 623. Ion-channel based formulation of the action potential 653.1 Ion-channel structure 653.2 Markov models of ion-channel kinetics 663.3 Role of selected ion channels in rate dependence of the cardiac action potential 713.4 Physiological implications of IKs subunit interaction 773.5 Mechanism of cardiac action potential rate-adaptation is species dependent 784. Simulating ion-channel mutations and their electrophysiological consequences 814.1 Mutations in SCN5A, the gene that encodes the cardiac sodium channel 824.1.1 The ΔKPQ mutation and LQT3 824.1.2 SCN5A mutation that underlies a dual phenotype 874.2 Mutations in HERG, the gene that encodes IKr: re-examination of the ‘gain of function/loss of function’ concept 944.3 Role of IKs as ‘repolarization reserve’ 1005. Modeling cell signaling in electrophysiology 1025.1 CaMKII regulation of the Ca2+ transient 1025.2 The β-adrenergic signaling cascade 1056. Epilogue 1077. Acknowledgments 1088. References 109The cardiac cell is a complex biological system where various processes interact to generate electrical excitation (the action potential, AP) and contraction. During AP generation, membrane ion channels interact nonlinearly with dynamically changing ionic concentrations and varying transmembrane voltage, and are subject to regulatory processes. In recent years, a large body of knowledge has accumulated on the molecular structure of cardiac ion channels, their function, and their modification by genetic mutations that are associated with cardiac arrhythmias and sudden death. However, ion channels are typically studied in isolation (in expression systems or isolated membrane patches), away from the physiological environment of the cell where they interact to generate the AP. A major challenge remains the integration of ion-channel properties into the functioning, complex and highly interactive cell system, with the objective to relate molecular-level processes and their modification by disease to whole-cell function and clinical phenotype. In this article we describe how computational biology can be used to achieve such integration. We explain how mathematical (Markov) models of ion-channel kinetics are incorporated into integrated models of cardiac cells to compute the AP. We provide examples of mathematical (computer) simulations of physiological and pathological phenomena, including AP adaptation to changes in heart rate, genetic mutations in SCN5A and HERG genes that are associated with fatal cardiac arrhythmias, and effects of the CaMKII regulatory pathway and β-adrenergic cascade on the cell electrophysiological function.
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ANDERSON, PETER A. V., and M. CRAIG MCKAY. "The Electrophysiology of Cnidocytes." Journal of Experimental Biology 133, no. 1 (1987): 215–30. http://dx.doi.org/10.1242/jeb.133.1.215.
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Electrical properties of cnidocytes isolated from the hydroid Cladonema and the scyphomedusa Chrysaora were examined using current- and voltage-clamp recording techniques. The stenoteles of Cladonema produced action potentials when depolarized above 0 m V. The inward current that produced the action potential was a Na+ current. These cells also possessed an A-current and a K-current. Atrichous isorhizas from Chrysaora did not spike and did not have any inward currents. All cells examined had K-currents, some had A-currents also. Very few cnidocytes discharged during the course of the recordings, irrespective of the degree to which they were depolarized or hyperpolarized, or the presence or selective blockade of any ionic currents. When discharge did occur it could never be correlated with any obvious electrophysiological event. Recordings from cnidocytes in situ in tentacles of the siphonophore Physalia indicate that these cells do not spike. Their current/voltage relationships were linear. They too did not discharge in response to changes in membrane potential, suggesting that the failure of isolated cnidocytes to discharge cannot be attributed to the isolation procedure.
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Shimmen, Teruo. "Involvement of receptor potentials and action potentials in mechano-perception in plants." Functional Plant Biology 28, no. 7 (2001): 567. http://dx.doi.org/10.1071/pp01038.
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The rapid turgor movements of Mimosa pudica and some carnivorous plants have long stimulated the interest of botanists. In addition, it is becoming evident that slower responses of plants to mechanical stimuli, such as coiling of tendrils and thigmomorphogenesis, are common phenomena. Electrophysiological studies on mechano-perception have been carried out in M. pudica and carnivorous plants, and have established that the response to mechanical stimulation is composed of three steps: perception of the stimulus, transmission of the signal, and induction of movement in motor cells. The first step is due to the receptor potential, the second and third steps are mediated by the action potential. In this article, the mechanisms of responses to mechanical stimuli of these plants are considered. Since higher plants are composed of complex tissues, detailed analysis of electrical phenomena is rather difficult, and so the mechanism for generating the receptor potential had not yet been studied. Characean cells have proved to be more amenable to the study of the electrophysiology of plant membranes because of their large cell size and the ease by which single cells can be isolated. Recent progress in studies of the receptor potential in characean cells is also discussed.
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Cherry, Elizabeth M., and Flavio H. Fenton. "A tale of two dogs: analyzing two models of canine ventricular electrophysiology." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (2007): H43—H55. http://dx.doi.org/10.1152/ajpheart.00955.2006.
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The extensive development of detailed mathematical models of cardiac myocyte electrophysiology in recent years has led to a proliferation of models, including many that model the same animal species and specific region of the heart and thus would be expected to have similar properties. In this paper we review and compare two recently developed mathematical models of the electrophysiology of canine ventricular myocytes. To clarify their similarities and differences, we also present studies using them in a range of preparations from single cells to two-dimensional tissue. The models are compared with each other and with new and previously published experimental results in terms of a number of their properties, including action potential morphologies; transmembrane currents during normal heart rates and during alternans; alternans onsets, magnitudes, and cessations; and reentry dynamics of spiral waves. Action potential applets and spiral wave movies for the two canine ventricular models are available online as supplemental material. We find a number of differences between the models, including their rate dependence, alternans dynamics, and reentry stability, and a number of differences compared with experiments. Differences between models of the same species and region of the heart are not unique to these canine models. Similar differences can be found in the behavior of two models of human ventricular myocytes and of human atrial myocytes. We provide several possible explanations for the differences observed in models of the same species and region of the heart and discuss the implications for the applicability of models in addressing questions of mechanism in cardiac electrophysiology.
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Enoka, Roger M., Ioannis G. Amiridis, and Jacques Duchateau. "Electrical Stimulation of Muscle: Electrophysiology and Rehabilitation." Physiology 35, no. 1 (2020): 40–56. http://dx.doi.org/10.1152/physiol.00015.2019.
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The generation of action potentials in intramuscular motor and sensory axons in response to an imposed external current source can evoke muscle contractions and elicit widespread responses throughout the nervous system that impact sensorimotor function. The benefits experienced by individuals exposed to several weeks of treatment with electrical stimulation of muscle suggest that the underlying adaptations involve several physiological systems, but little is known about the specific changes elicited by such interventions.
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Saito, Mitsuyoshi L. "NanoTouch: intracellular recording using transmembrane conductive nanoparticles." Journal of Neurophysiology 122, no. 5 (2019): 2016–26. http://dx.doi.org/10.1152/jn.00359.2019.
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Observations of the electrophysiological properties of cells are important for understanding cellular functions and their underlying mechanisms. Short action potentials in axons are essential to rapidly deliver signals from the neuronal cell body to the terminals, whereas longer action potentials are required for sufficient calcium influx for transmitter release at the synaptic terminals and for cardiomyocyte and smooth muscle contractions. To accurately observe the shape and timing of depolarizations, it is essential to measure changes in the intracellular membrane potential. The ability to record action potentials and intracellular membrane potentials from mammalian cells and neurons was made possible by Ling and Gerard’s discovery in 1949, when they introduced sharp glass electrode with a submicron sized tip. Because of the small tip size, the sharp glass electrode could penetrate the cell membrane with little damage, which was one of the major breakthroughs in cellular electrophysiology and is the basic principle of the intracellular recording technique to date, providing the basis for further innovation of patch-clamp electrophysiology. I report a proof-of-principle demonstration of a novel method for recording intracellular potentials without penetrating the cell membrane using glass electrodes. We discovered that magnetically held transmembrane conductive nanoparticles can function as an intracellular electrode to detect transmembrane membrane potentials similar to those obtained by the conventional patch-clamp recording method. NEW & NOTEWORTHY To accurately observe the shape of action potentials, it is essential to perform intracellular recordings. I present a method to record intracellular potentials using magnetically held magnetic conductive nanoparticles in the membrane as an electrode. These nanoparticles function similarly to a conventional intracellular microelectrode. This is the first report to apply conductive nanoparticles to detect action potentials in the form of electrical signals.
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Andersen, O. S., and R. E. Koeppe. "Molecular determinants of channel function." Physiological Reviews 72, suppl_4 (1992): S89—S158. http://dx.doi.org/10.1152/physrev.1992.72.suppl_4.s89.
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The 40 years since the seminal papers of Hodgkin and Huxley appeared have been extraordinarily productive in terms of understanding the molecular basis for electrical activity. The Hodgkin-Huxley proposal that electrical excitability should be understood in terms of voltage-dependent changes in discrete sites has been resoundingly verified. Indeed, the Hodgkin-Huxley framework is remarkable in that its essential elements have remained largely intact as molecular understanding has advanced. This robustness is, at least in part, a result of the fact that Hodgkin and Huxley developed a mathematical model, based on simple physical arguments, that was sufficiently comprehensive to describe the kinetics of the voltage-clamped currents and yet simple enough to be predictive. The predictive features were demonstrated early by the reconstruction of both space-clamped and propagated action potentials on a desk-top calculator (293) and, later, when the sites of Hodgkin and Huxley developed into being well-characterized molecular structures. Voltage- and ligand-dependent ion-selective channels are now the established framework within which cellular electrophysiology is being pursued. Moreover, electrophysiological measurements of membrane and single-channel currents have become essential tools to examine molecular questions pertaining to channel structure and activity. The last 10 years have witnessed spectacular activity, which has resulted from two developments, the giga-seal patch clamp (249) and the elucidation of primary sequences of a number of channel-forming proteins (494), along with the first outlines of their low-resolution three-dimensional structures (651). The stage is now set for 1) applying a variety of convergent techniques to decipher molecular structural details at high resolution, and 2) seeking to understand the complex dynamic functions, gating, and ion selectivity at the molecular level. The early successes are likely to be in understanding the molecular determinants of ion conductance and selectivity, initially in terms of quantitative descriptions of how a sequence modification can alter a channel's permeability characteristics. Channel gating is a far more elusive target because it involves molecular rearrangements, which are poorly understood at any level of description and which may be modified by the channel's environment. The general mechanisms of ion permeation and gating will differ among different classes of ion channels, but a molecular understanding of either phenomenon must eventually be based on an understanding of intermolecular forces, which are invariant among all channel types.(ABSTRACT TRUNCATED AT 400 WORDS)
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Lurie, K. G., T. M. Argentieri, J. Sheldon, L. H. Frame, and F. M. Matschinsky. "Metabolism and electrophysiology in subendocardial Purkinje fibers after infarction." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 3 (1987): H662—H670. http://dx.doi.org/10.1152/ajpheart.1987.253.3.h662.
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Subendocardial Purkinje fibers (SEPF) have been implicated in the genesis of fatal arrhythmias that occur 24-48 h after infarction but little is known about the metabolic processes involved. Quantitative microchemical and electrophysiological studies were performed on normal and infarcted hearts removed 24 h after coronary artery occlusion. ATP, ADP, AMP, total adenine nucleotide content, phosphocreatine (PCr), and inorganic phosphate in superficial subendocardial Purkinje fibers from infarct preparations decreased approximately 30% compared with normal preparations. The phosphate potential decreased 45% in the infarct group. Similar changes were observed in adjacent contractile muscle between normals and infarcts. Action potentials of SEPF from infarct hearts had increased automaticity, markedly prolonged action potential durations at 50 and 90% repolarization (APD50 or APD90), but unchanged resting membrane potentials. The decrease in ATP, total adenine nucleotides, and the phosphate potential correlated linearly with APD50 and APD90. No correlation was found between PCr and APD90. This combined biochemical and electrophysiological approach provides a promising new way to further probe the biochemical basis of the abnormal electrical properties of subendocardial Purkinje fibers after myocardial infarction.
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Ravens, Ursula. "Sex differences in cardiac electrophysiology." Canadian Journal of Physiology and Pharmacology 96, no. 10 (2018): 985–90. http://dx.doi.org/10.1139/cjpp-2018-0179.
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Women have a longer QT interval than men, which appears to evolve after puberty suggesting that sex hormones have an influence on cardiac electrophysiology. Sex hormones do in fact regulate cardiac ion channels via genomic and nongenomic pathways. Women are at greater risk for life-threatening arrhythmias under conditions that prolong the QT interval. In addition, women exhibit greater sensitivity to QT interval–prolonging drugs. Female sex has also an impact on propensity to cardiovascular disease, including atrial fibrillation. However, ex vivo recorded atrial action potentials (APs) from female and male patients in atrial fibrillation did not exhibit significant differences in shape, except that APs from women had slower upstroke velocity. It is concluded that sex-related differences should be taken into account not only in the clinics, but also in basic research.
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Wann, K. T. "The electrophysiology of the somatic muscle cells of Ascaris suum and Ascaridia galli." Parasitology 94, no. 3 (1987): 555–66. http://dx.doi.org/10.1017/s003118200005589x.
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The electrophysiological properties of the bag region of the somatic muscle cells of Ascaris suum and Ascaridia galli were studied using intracellular techniques. For Ascaris muscle cells, the mean resting membrane potentials at 20 and 37°C were −29·9 and −33·8 mV respectively, and the average input conductance was 2·12 μS. For the muscle cells of A. galli similar values were obtained. For example, the mean input conductance of these cells was 2·84 μS at 20°C. Healthy Ascaris muscle cells at near physiological temperatures show both spontaneous depolarizing and hyperpolarizing activity and, in cells close to the nerve cords, rhythmic large amplitude (approximately 30 mV) action potentials are observed. Such action potentials, which are very sensitive to temperature variations, originate in the muscle cells. In contrast the muscle cells of Ascaridia are quiescent. The rhythmic action potentials of Ascaris are resistant to tetrodotoxin (TTX) (≤ 10−6 M), verapamil (10−4 M) and cinnarizine (10−4 M), but are blocked irreversibly by 22, 23 dihydroavermectin B1a (10−7 to 5 × 10−6 M). GABA, and the GABAA receptor agonists, muscimol and isoguvacine, hyperpolarize and increase the input conductance of both Ascaris and Ascaridia muscle cells. The antagonists+bicuculline and picrotoxin were not effective in modulating the spontaneous hyper polarizations of Ascaris muscle cells, and picrotoxin (10−4 M) was not effective in altering the response to GABA (5 × 10−6 M). The significance of the results is discussed briefly.
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Iturriaga, Renato, and Héctor Sánchez-Morgado. "Finsler metrics and action potentials." Proceedings of the American Mathematical Society 128, no. 11 (2000): 3311–16. http://dx.doi.org/10.1090/s0002-9939-00-05710-5.
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McCormick, D. A., B. W. Connors, J. W. Lighthall, and D. A. Prince. "Comparative electrophysiology of pyramidal and sparsely spiny stellate neurons of the neocortex." Journal of Neurophysiology 54, no. 4 (1985): 782–806. http://dx.doi.org/10.1152/jn.1985.54.4.782.
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Slices of sensorimotor and anterior cingulate cortex from guinea pigs were maintained in vitro and bathed in a normal physiological medium. Electrophysiological properties of neurons were assessed with intracellular recording techniques. Some neurons were identified morphologically by intracellular injection of the fluorescent dye Lucifer yellow CH. Three distinct neuronal classes of electrophysiological behavior were observed; these were termed regular spiking, bursting, and fast spiking. The physiological properties of neurons from sensorimotor and anterior cingulate areas did not differ significantly. Regular-spiking cells were characterized by action potentials with a mean duration of 0.80 ms at one-half amplitude, a ratio of maximum rate of spike rise to maximum rate of fall of 4.12, and a prominent afterhyperpolarization following a train of spikes. The primary slope of initial spike frequency versus injected current intensity was 241 Hz/nA. During prolonged suprathreshold current pulses the frequency of firing adapted strongly. When local synaptic pathways were activated, all cells were transiently excited and then strongly inhibited. Bursting cells were distinguished by their ability to generate endogenous, all-or-none bursts of three to five action potentials. Their properties were otherwise very similar to regular-spiking cells. The ability to generate a burst was eliminated when the membrane was depolarized to near the firing threshold with tonic current. By contrast, hyperpolarization of regular-spiking (i.e., nonbursting) cells did not uncover latent bursting tendencies. The action potentials of fast-spiking cells were much briefer (mean of 0.32 ms) than those of the other cell types.(ABSTRACT TRUNCATED AT 250 WORDS)
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Li, Q., Z. Guan, B. A. Biagi, B. T. Stokes, and R. A. Altschuld. "Hyperthyroid adult rat cardiomyocytes. II. Single cell electrophysiology and free calcium transients." American Journal of Physiology-Cell Physiology 257, no. 5 (1989): C957—C963. http://dx.doi.org/10.1152/ajpcell.1989.257.5.c957.
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The effects of hyperthyroidism on electrophysiological properties and intracellular free calcium transients in single adult rat cardiomyocytes were studied using conventional microelectrodes and time-resolved single cell fura-2 fluorescence microscopy. Under control conditions, resting membrane potentials and triggered action potentials were not different in euthyroid and hyperthyroid myocytes. Calcium transients produced by electrical stimulation, however, were markedly abbreviated in hyperthyroid myocytes. During a train of stimuli, the duration of the calcium transients at half peak amplitude (half time) was 124 +/- 14 ms at the fifth beat in hyperthyroid cells vs. 287 +/- 35 ms in euthyroid cells. Isoproterenol (1 microM) prolonged time to 50% repolarization (APD50) of the action potentials and increased the peak calcium transients in both euthyroid and hyperthyroid myocytes. It also shortened the half time of the calcium transients in euthyroid myocytes but had little effect on the half time in hyperthyroid cells. These data are consistent with the electrophysiology and mechanical performance in intact euthyroid and hyperthyroid cardiac tissues, and the intrinsic changes in hyperthyroid tissues can therefore be illustrated in single ventricular myocytes. Furthermore, the results suggest that alterations in intracellular calcium handling by sarcoplasmic reticulum may account for contractile changes of the heart induced by hyperthyroidism.
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Rozanski, G. J., and S. L. Lipsius. "Electrophysiology of functional subsidiary pacemakers in canine right atrium." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 3 (1985): H594—H603. http://dx.doi.org/10.1152/ajpheart.1985.249.3.h594.
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Glass microelectrodes were used to study the electrical activity of the subsidiary atrial pacemaker (SAP) cells that maintain atrial excitation after suppression of the sinoatrial node. Tissues with documented SAP activity were isolated from the canine inferior right atrium and superfused in vitro with Tyrode solution containing norepinephrine (NE, 10(-8)-10(-7) M). SAP action potentials exhibited prominent diastolic depolarization and a significantly lower maximum diastolic potential, take-off potential, overshoot, rate of rise, and amplitude than typical atrial muscle. Withdrawal of NE completely blocked SAP propagation, although SAP automaticity continued at a slower rate. Acetylcholine (ACh, 5 X 10(-8) M) usually produced complete exit block and decreased spontaneous rate. Higher concentrations of ACh (10(-6) M) elicited a prominent hyperpolarization (19.2 +/- 6.6 mV), completely suppressing SAP automaticity. In quiescent preparations exposed to NE greater than or equal to 10(-7) M, external stimuli at short cycle lengths (less than 1,000 ms) elicited action potentials with delayed afterdepolarizations, which frequently caused nondriven repetitive activity. This triggered activity was inhibited by verapamil or withdrawal of NE. These studies identify and characterize the electrical activity of functional subsidiary pacemakers located in a specific region of the inferior right atrium. In addition, fibers within this region display triggered activity. Spontaneous activity generated by fibers within the SAP region may cause atrial dysrhythmias.
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Jia, Xiaoxuan, Joshua H. Siegle, Corbett Bennett, et al. "High-density extracellular probes reveal dendritic backpropagation and facilitate neuron classification." Journal of Neurophysiology 121, no. 5 (2019): 1831–47. http://dx.doi.org/10.1152/jn.00680.2018.
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Different neuron types serve distinct roles in neural processing. Extracellular electrical recordings are extensively used to study brain function but are typically blind to cell identity. Morphoelectrical properties of neurons measured on spatially dense electrode arrays have the potential to distinguish neuron types. We used high-density silicon probes to record from cortical and subcortical regions of the mouse brain. Extracellular waveforms of each neuron were detected across many channels and showed distinct spatiotemporal profiles among brain regions. Classification of neurons by brain region was improved with multichannel compared with single-channel waveforms. In visual cortex, unsupervised clustering identified the canonical regular-spiking (RS) and fast-spiking (FS) classes but also indicated a subclass of RS units with unidirectional backpropagating action potentials (BAPs). Moreover, BAPs were observed in many hippocampal RS cells. Overall, waveform analysis of spikes from high-density probes aids neuron identification and can reveal dendritic backpropagation. NEW & NOTEWORTHY It is challenging to identify neuron types with extracellular electrophysiology in vivo. We show that spatiotemporal action potentials measured on high-density electrode arrays can capture cell type-specific morphoelectrical properties, allowing classification of neurons across brain structures and within the cortex. Moreover, backpropagating action potentials are reliably detected in vivo from subpopulations of cortical and hippocampal neurons. Together, these results enhance the utility of dense extracellular electrophysiology for cell-type interrogation of brain network function.
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McQuiston, A. Rory, and Lawrence C. Katz. "Electrophysiology of Interneurons in the Glomerular Layer of the Rat Olfactory Bulb." Journal of Neurophysiology 86, no. 4 (2001): 1899–907. http://dx.doi.org/10.1152/jn.2001.86.4.1899.
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In the mammalian olfactory bulb, glomeruli are surrounded by a heterogeneous population of interneurons called juxtaglomerular neurons. As they receive direct input from olfactory receptor neurons and connect with mitral cells, they are involved in the initial stages of olfactory information processing, but little is known about their detailed physiological properties. Using whole cell patch-clamp techniques, we recorded from juxtaglomerular neurons in rat olfactory bulb slices. Based on their response to depolarizing pulses, juxtaglomerular neurons could be divided into two physiological classes: bursting and standard firing. When depolarized, the standard firing neurons exhibited a range of responses: accommodating, nonaccommodating, irregular firing, and delayed to firing patterns of action potentials. Although the firing pattern was not rigorously predictive of a particular neuronal morphology, most short axon cells fired accommodating trains of action potentials, while most delayed to firing cells were external tufted cells. In contrast to the standard firing neurons, bursting neurons produced a calcium-channel-dependent low-threshold spike when depolarized either by current injection or by spontaneous or evoked postsynaptic potentials. Bursting neurons also could oscillate spontaneously. Most bursting cells were either periglomerular cells or external tufted cells. Based on their mode of firing and placement in the bulb circuit, these bursting cells are well situated to drive synchronous oscillations in the olfactory bulb.
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Laurita, Kenneth R., and Ashish Singal. "Mapping action potentials and calcium transients simultaneously from the intact heart." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (2001): H2053—H2060. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2053.
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Intracellular calcium handling plays an important role in cardiac electrophysiology. Using two fluorescent indicators, we developed an optical mapping system that is capable of measuring calcium transients and action potentials at 256 recording sites simultaneously from the intact guinea pig heart. On the basis of in vitro measurements of dye excitation and emission spectra, excitation and emission filters at 515 ± 5 and >695 nm, respectively, were used to measure action potentials with di-4-ANEPPS, and excitation and emission filters at 365 ± 25 and 485 ± 5 nm, respectively, were used to measure calcium transients with indo 1. The percent error due to spectral overlap was small when action potentials were measured (1.7 ± 1.0%, n = 3) and negligible when calcium transients were measured (0%, n = 3). Recordings of calcium transients, action potentials, and isochrone maps of depolarization time and the time of calcium transient onset indicated negligible error due to fluorescence emission overlap. These data demonstrate that the error due to spectral overlap of indo 1 and di-4-ANEPPS is sufficiently small, such that optical mapping techniques can be used to measure calcium transients and action potentials simultaneously in the intact heart.
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Eckardt, Lars, Andreas Meißner, Paulus Kirchhof, et al. "In vivo recording of monophasic action potentials in awake dogs - new applications for experimental electrophysiology." Basic Research in Cardiology 96, no. 2 (2001): 169–74. http://dx.doi.org/10.1007/s003950170067.
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Zhang, Youhua, and Todor N. Mazgalev. "Foot formation in action potentials from atrioventricular nodal cells: Rosenblueth hypothesis or dual pathway electrophysiology?" Heart Rhythm 2, no. 5 (2005): S140. http://dx.doi.org/10.1016/j.hrthm.2005.02.437.
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Nambu, A., and R. Llinas. "Electrophysiology of globus pallidus neurons in vitro." Journal of Neurophysiology 72, no. 3 (1994): 1127–39. http://dx.doi.org/10.1152/jn.1994.72.3.1127.
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1. We investigated the electrical properties of globus pallidus neurons intracellularly using brain slices from adult guinea pigs. Three types of neurons were identified according to their intrinsic electrophysiological properties. 2. Type I neurons (59%) were silent at the resting membrane level (-65 +/- 10 mV, mean +/- SD) and generated a burst of spikes, with strong accommodation, to depolarizing current injection. Calcium-dependent low-frequency (1-8 Hz) membrane oscillations were often elicited by membrane depolarization (-53 +/- 8 mV). A low-threshold calcium conductance and an A-current were also identified. The mean input resistance of this neuronal type was 70 +/- 22 M omega. 3. Type II neurons (37%) fired spontaneously at the resting membrane level (-59 +/- 9 mV). Their repetitive firing (< or = 200 Hz) was very sensitive to the amplitude of injected current and showed weak accommodation. Sodium-dependent high-frequency (20-100 Hz) subthreshold membrane oscillations were often elicited by membrane depolarization. This neuronal type demonstrated a low-threshold calcium spike and had the highest input resistance (134 +/- 62 M omega) of the three neuron types. 4. Type III neurons (4%) did not fire spontaneously at the resting membrane level (-73 +/- 5 mV). Their action potentials were characterized by a long duration (2.3 +/- 0.6 ms). Repetitive firing elicited by depolarizing current injection showed weak or no accommodation. This neuronal type had an A-current and showed the lowest input resistance (52 +/- 35 M omega) of the three neuron types. 5. Stimulation of the caudoputamen evoked inhibitory postsynaptic potentials (IPSPs) in Type I and II neurons. In Type II neurons the IPSPs were usually followed by rebound firing. Excitatory postsynaptic potentials and antidromic responses were also elicited in some Type I and II neurons. The estimated conduction velocity of the striopallidal projection was < 1 m/s (Type I neurons, 0.49 +/- 0.37 m/s; Type II neurons, 0.33 +/- 0.13 m/s).
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FEBVRE-CHEVALIER, COLETTE, ANDRÉ BILBAUT, QUENTIN BONE, and JEAN FEBVRE. "Sodium-Calcium Action Potential Associated with Contraction in the Heliozoan Actinocoryne Contractilis." Journal of Experimental Biology 122, no. 1 (1986): 177–92. http://dx.doi.org/10.1242/jeb.122.1.177.
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The electrophysiology of the contractile protozoan Actinocoryne contractilis was studied with conventional intracellular recording techniques. Resting membrane potential (−78 mV, s.d. = 8, N = 18) was dependent upon external K+. Rapid action potentials (overshoot up to 50 mV) were evoked either by mechanical stimulation or by current injection. Graded membrane depolarizations induced by graded mechanical stimuli correspond to receptor potentials. The receptor potential was mainly Na+-dependent; the action potential was also mainly Na+-dependent, but involved a minor Ca2+-dependence. The two components of the action potential could be separated in Ca2+-free solution containing EGTA (1 mmol l−1), in low-Na+ solutions or by the addition of Co2+. The repolarizing phase of the action potential was sensitive to TEA ions and to 4-aminopyridine (4-AP). Action potentials were followed in 10–20 ms by a rapid all-or-none contraction of the axopods and stalk. Contraction was blocked in Ca2+-free solution containing EGTA and by Co2+, which suggests a requirement of external Ca2+ for this event. Contraction was also abolished by 4-AP.
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Leudar, Augustine. "Surrounded: A Series of Sound Installations That Combine Plant Electrophysiology and 3D Sonic Art." Leonardo 51, no. 5 (2018): 517–23. http://dx.doi.org/10.1162/leon_a_01338.
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This paper discusses a series of sound installations that combine plant electrophysiology with 3D sonic art. A brief introduction to plant electrophysiology is given. The sonification of electrophysiological signals in the mycorrhizal network is discussed, explaining how art and science are combined in this project in a way that differs from the simple sonification of data. Novel 3D audio spatialization techniques, the 3D audio mapping of natural environments and immersion are also discussed, along with technical details of how to read the electrical signals in plants known as action potentials. Other topics addressed include acoustic signaling in the forest, spectral composition and interaction with forest flora and fauna.
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Battista, Nicholas Anthony, and Laura Ann Miller. "Bifurcations in valveless pumping techniques from a coupled fluid-structure-electrophysiology model in heart development." BIOMATH 6, no. 2 (2017): 1711297. http://dx.doi.org/10.11145/j.biomath.2017.11.297.
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We explore an embryonic heart model that couples electrophysiology and muscle-force generation to flow induced using a $2D$ fluid-structure interaction framework based on the immersed boundary method. The propagation of action potentials are coupled to muscular contraction and hence the overall pumping dynamics. In comparison to previous models, the electro-dynamical model does not use prescribed motion to initiate the pumping motion, but rather the pumping dynamics are fully coupled to an underlying electrophysiology model, governed by the FitzHugh-Nagumo equations. Perturbing the diffusion parameter in the FitzHugh-Nagumo model leads to a bifurcation in dynamics of action potential propagation. This bifurcation is able to capture a spectrum of different pumping regimes, with dynamic suction pumping and peristaltic-like pumping at the extremes. We find that more bulk flow is produced within the realm of peristaltic-like pumping.
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Kujtan, Peter W., and Peter L. Carlen. "Phencyclidine actions measured intracellularly in hippocampal CA1 neurons." Canadian Journal of Physiology and Pharmacology 68, no. 10 (1990): 1351–56. http://dx.doi.org/10.1139/y90-204.
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The electrophysiological effects of phencyclidine (PCP) were measured intracellularly in guinea pig hippocampal CA1 neurons in vitro. At all doses tested (0.2 μM – 10 mM), PCP increased the width of action potentials (APs). Doses of 10 μM and higher were associated with decreased action potential amplitude. PCP decreased inhibitory postsynaptic potentials and excitatory postsynaptic potentials but did not alter responses to focally applied GABA. At the lowest dose (0.2 μM), PCP decreased the input resistance (Rin), while at all other doses Rin was increased. PCP decreased post-spike train afterhyperpolarizations at low and medium doses. PCP effects persisted in low calcium medium and also in medium containing 10−6 M tetrodotoxin. It is concluded that in these central neurons, PCP primarily blocks potassium conductances at all doses and, at anesthetic doses, depresses sodium-dependent spikes.Key words: phencyclidine, potassium conductance, CA1 neurons, electrophysiology.
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Duker, G., P. O. Sjoquist, and B. W. Johansson. "Monophasic action potentials during induced hypothermia in hedgehog and guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (1987): H1083—H1088. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1083.
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To evaluate mechanisms behind the difference in susceptibility to ventricular fibrillation (VF) between the guinea pig and hedgehog heart, the cardiac electrophysiology of the two species was studied at normal body temperature and at different hypothermic levels by simultaneous recording of the monophasic action potential (MAP) and the external electrocardiogram (ECG). At normal body temperature, the duration of the ventricular MAP was significantly shorter in the hedgehog (93 +/- 8.1 ms) than in the guinea pig (138 +/- 2.6 ms). There was a distinct plateau phase in the guinea pig, whereas no such phase could be detected in the hedgehog. During hypothermia, a similar increase in MAP duration at full repolarization was noticed for both species. However, the prolongation of the MAP at lower repolarization levels was much less in the hedgehog. Besides, hypothermia-induced slow conduction and dispersion of ventricular repolarization was much more apparent in the guinea pig heart compared with the hedgehog heart. These differences may be important factors in the resistance to VF in the hedgehog, at normal body temperature and during hypothermia.
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Llinás, R., and J. Lopez-Barneo. "Electrophysiology of mammalian tectal neurons in vitro. II. Long-term adaptation." Journal of Neurophysiology 60, no. 3 (1988): 869–78. http://dx.doi.org/10.1152/jn.1988.60.3.869.
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1. The long-term adaptation of repetitive firing in guinea pig superior colliculus neurons was studied in a mesencephalic slice preparation using intracellular recording techniques. 2. This long-term adaptation was characterized by a decrease in the number of action potentials generated by a depolarizing pulse of constant amplitude applied at frequencies of 0.5-2 Hz. Long-term adaptation appeared in all cells tested regardless of whether they showed short-term spike frequency adaptation during each pulse. 3. Long-term adaptation had a close-to-exponential time course with a time constant of 4.085 +/- 0.675 s (mean +/- SD, n = 8). This phenomenon developed more rapidly as the stimulus frequency increased and was paralleled by a progressive hyperpolarization of the membrane potential which, at the termination of the train of stimuli, remained 6-10 mV more negative than the resting value. 4. The hyperpolarization and the spike frequency adaptation recovered spontaneously in approximately 60 s. The time constant of recovery was 14.66 +/- 1.189 s (n = 4). 5. The afterhyperpolarization (AHP) was also paralleled by a decrease in the input resistance of the cells. This response and the adaptation disappeared after removal of Ca2+ or after addition of Cd2+ to the external solution. This suggests that Ca2+ entry during trains of action potentials activates a Ca2+-dependent K+ conductance with an unusually slow kinetics. 6. This conductance appears to differ from other Ca2+-dependent K+ conductances in that it was blocked by 4-aminopyridine. 7. The properties of this long-term adaptation are remarkably similar to those reported for visual habituation; thus this newly described K+ conductance may be pertinent to the understanding of this behavioral phenomenon.
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Mills, William R., Niladri Mal, Farhad Forudi, Zoran B. Popovic, Marc S. Penn, and Kenneth R. Laurita. "Optical mapping of late myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (2006): H1298—H1306. http://dx.doi.org/10.1152/ajpheart.00437.2005.
Full textAbstract:
Late myocardial infarction (MI) is associated with ventricular arrhythmias and sudden cardiac death. The exact mechanistic relationship between abnormal cellular electrophysiology, conduction abnormalities, and arrhythmogenesis associated with late MI is not completely understood. We report a novel, rapid dye superfusion technique to enable whole heart, high-resolution optical mapping of late MI. Optical mapping of action potentials was performed in normal rats and rats with anterior MI 7 days after left anterior descending artery ligation. Hearts from normal rats exhibited normal action potentials and impulse conduction. With the use of programmed stimulation to assess arrhythmia inducibility, 29% of hearts with late MI had inducible sustained ventricular tachycardia, compared with 0% in normal rats. A causal relationship between the site of infarction, abnormal action potential conduction (i.e., block and slow conduction), and arrhythmogenesis was observed. Optical mapping techniques can be used to measure high-resolution action potentials in a whole heart model of late MI. This experimental model reproduces many of the electrophysiological characteristics (i.e., conduction slowing, block, and ventricular tachycardia) associated with MI in patients. Importantly, the results of this study can enhance our ability to understand the interplay between cellular heterogeneity, conduction abnormalities, and arrhythmogenesis associated with MI.
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Rasmusson, R. L., J. W. Clark, W. R. Giles, E. F. Shibata, and D. L. Campbell. "A mathematical model of a bullfrog cardiac pacemaker cell." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 2 (1990): H352—H369. http://dx.doi.org/10.1152/ajpheart.1990.259.2.h352.
Full textAbstract:
Previous models of cardiac cellular electrophysiology have been based largely on voltage-clamp measurements obtained from multicellular preparations and often combined data from different regions of the heart and a variety of species. We have developed a model of cardiac pacemaking based on a comprehensive set of voltage-clamp measurements obtained from single cells isolated from one specific tissue type, the bullfrog sinus venosus (SV). Consequently, sarcolemmal current densities and kinetics are not influenced by secondary phenomena associated with multicellular preparations, allowing us to realistically simulate processes thought to be important in pacemaking, including the Na(+)-K+ pump and Na(+)-Ca2+ exchanger. The membrane is surrounded extracellularly by a diffusion-limited space and intracellularly by a limited myoplasmic volume containing Ca2(+)-binding proteins (calmodulin, troponin). The model makes several predictions regarding mechanisms involved in pacing. 1) Primary pacemaking cannot be attributed to any single current but arises from both the lack of a background K+ current and a complex interaction between Ca2+, delayed-rectifier K+, and background leak currents. 2) Ca2+ current displays complex behavior and is important during repolarization. 3) Because of Ca2+ buffering by myoplasmic proteins, the Na(+)-Ca2+ exchanger current is small and has little influence on action potential repolarization but may modulate the maximum diastolic potential. 4) The Na(+)-K+ pump current does not play an active role in repolarization but is of sufficient size to modulate the rate of diastolic depolarization. 5) K+ accumulation and Ca2+ depletion may occur in the extracellular spaces but play no role in either the diastolic depolarization or repolarization of a single action potential. This model illustrates the importance of basing simulations on quantitative measurements of ionic currents in myocytes and of including both electrogenic transporter mechanisms and Ca2+ buffering by myoplasmic Ca2(+)-binding proteins.
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Dwyer, T. M., J. Fleming, J. E. Randall, and T. G. Coleman. "Teaching physiology and the World Wide Web: electrochemistry and electrophysiology on the Internet." Advances in Physiology Education 273, no. 6 (1997): S2. http://dx.doi.org/10.1152/advances.1997.273.6.s2.
Full textAbstract:
Students seek active learning experiences that can rapidly impart relevant information in the most convenient way possible. Computer-assisted education can now use the resources of the World Wide Web to convey the important characteristics of events as elemental as the physical properties of osmotically active particles in the cell and as complex as the nerve action potential or the integrative behavior of the intact organism. We have designed laboratory exercises that introduce first-year medical students to membrane and action potentials, as well as the more complex example of integrative physiology, using the dynamic properties of computer simulations. Two specific examples are presented. The first presents the physical laws that apply to osmotic, chemical, and electrical gradients, leading to the development of the concept of membrane potentials; this module concludes with the simulation of the ability of the sodium-potassium pump to establish chemical gradients and maintain cell volume. The second module simulates the action potential according to the Hodgkin-Huxley model, illustrating the concepts of threshold, inactivation, refractory period, and accommodation. Students can access these resources during the scheduled laboratories or on their own time via our Web site on the Internet (http./(/)phys-main.umsmed.edu) by using the World Wide Web protocol. Accurate version control is possible because one valid, but easily edited, copy of the labs exists at the Web site. A common graphical interface is possible through the use of the Hypertext mark-up language. Platform independence is possible through the logical and arithmetic calculations inherent to graphical browsers and the Javascript computer language. The initial success of this program indicates that medical education can be very effective both by the use of accurate simulations and by the existence of a universally accessible Internet resource.
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Costa, Andrea R., Nikhil C. Panda, Sandro Yong, et al. "Optical mapping of cryoinjured rat myocardium grafted with mesenchymal stem cells." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 1 (2012): H270—H277. http://dx.doi.org/10.1152/ajpheart.00019.2011.
Full textAbstract:
Mesenchymal stem cells (MSCs) have been shown to improve cardiac electrophysiology when administered in the setting of acute myocardial infarction. However, the electrophysiological phenotype of MSCs in situ is not clear. We hypothesize that MSCs delivered intramyocardially to cryoinjured myocardium can engraft, but will not actively generate, action potentials. Cryoinjury-induced scar was created on the left ventricular epicardial surface of adult rat hearts. Within 30 min, hearts were injected with saline (sham, n = 11) or bone marrow-derived MSCs (2 × 106) labeled with 1,1′-dioctadecyl-3,3,3,3′-tetramethylindocarbocyanine percholate (DiI; n = 16). At 3 wk, optical mapping and cell isolation were used to measure optical action potentials and calcium transients, respectively. Histological analysis confirmed subepicardial scar thickness and the presence of DiI-positive cells that express connexin-43. Optical action potential amplitude within the scar at MSC-positive sites (53.8 ± 14.3%) was larger compared with sites devoid of MSCs (35.3 ± 14.2%, P < 0.05) and sites within the scar of shams (33.5 ± 6.9%, P < 0.05). Evidence of simultaneous action potential upstroke, the loss of action potential activity following ablation of adjacent viable myocardium, and no rapid calcium transient response in isolated DiI+ cells suggest that the electrophysiological influence of engrafted MSCs is electrotonic. MSCs can engraft when directly injected into a cryoinjury and are associated with evidence of action potential activity. However, our results suggest that this activity is not due to generation of action potentials, but rather passive influence coupled from neighboring viable myocardium.
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Lopez-Barneo, J., and R. Llinas. "Electrophysiology of mammalian tectal neurons in vitro. I. Transient ionic conductances." Journal of Neurophysiology 60, no. 3 (1988): 853–68. http://dx.doi.org/10.1152/jn.1988.60.3.853.
Full textAbstract:
1. The electrophysiologic properties and ionic conductances of neurons located in the stratum griseum medium (SGM) of the guinea pig superior colliculus (SC) were studied by intracellular techniques in an in vitro mesencephalic slice preparation. 2. Cells were stained with Lucifer yellow and demonstrated a uniform appearance. They had an ovoid soma with dendrites directed toward the dorsal surface. These dendrites crossed the stratum opticum, and their fine ramifications reached the stratum zonale. 3. SGM cells had a mean resting potential of 59.4 +/- 5.1 (SE) mV (n = 30), a mean slope input resistance of 26.6 +/- 10 M omega (n = 30), and a mean time constant of 4.13 +/- 1.3 ms (n = 27). 4. Direct depolarization of SC neurons produced tonic repetitive firing. These Na+-dependent action potentials showed spike-frequency adaptation. After addition of tetrodotoxin (TTX) and replacement of Ca2+ by Ba2+, slow, high-threshold spikes were also generated. The trains of Ba2+ spikes did not show adaptation. 5. In about half of the cells direct hyperpolarization elicited a slow return of the membrane potential to base line at the termination of the pulse (probably due to activation of an A-type conductance) and no anomalous rectification. The remaining cells did not have an A-type conductance but demonstrated anomolous rectification which was reversibly abolished by Cs+ but unaffected by Ba2+. 6. Some cells could be anti- and/or orthodromically activated by a stimulating electrode placed at the intercollicular commissure. These, and action potentials elicited by direct activation, had a shoulder on their falling phase. The shoulder disappeared after removal of external Ca2+ or addition of Cd2+ to the bath. 7. During repetitive firing in those cells that demonstrated an A-type conductance, the shoulder became progressively more accentuated during the train of spikes, due to inactivation of this A-type conductance. This resulted in an increase in spike duration. 8. The electrophysiological properties of these cells and their morphological characteristics suggest that they may serve as the element integrating visual and nonvisual information at the superior colliculus.