Language：English   Publishing type：Research paper (scientific journal)   Publisher：Nature Publishing  

The cochlear lateral wall-an epithelial-like tissue comprising inner and outer layers-maintains +80 mV in endolymph. This endocochlear potential supports hearing and represents the sum of all membrane potentials across apical and basolateral surfaces of both layers. The apical surfaces are governed by K+ equilibrium potentials. Underlying extracellular and intracellular [K+] is likely controlled by the "circulation current," which crosses the two layers and unidirectionally flows throughout the cochlea. This idea was conceptually reinforced by our computational model integrating ion channels and transporters; however, contribution of the outer layer's basolateral surface remains unclear. Recent experiments showed that this basolateral surface transports K+ using Na+, K+-ATPases and an unusual characteristic of greater permeability to Na+ than to other ions. To determine whether and how these machineries are involved in the circulation current, we used an in silico approach. In our updated model, the outer layer's basolateral surface was provided with only Na+, K+-ATPases, Na+ conductance, and leak conductance. Under normal conditions, the circulation current was assumed to consist of K+ and be driven predominantly by Na+, K+-ATPases. The model replicated the experimentally measured electrochemical properties in all compartments of the lateral wall, and endocochlear potential, under normal conditions and during blocking of Na+, K+-ATPases. Therefore, the circulation current across the outer layer's basolateral surface depends primarily on the three ion transport mechanisms. During the blockage, the reduced circulation current partially consisted of transiently evoked Na+ flow via the two conductances. This work defines the comprehensive system driving the circulation current.

DOI： 10.1038/s41540-017-0025-0

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Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)   Publisher：日本心電学会  

Acetylcholine (ACh) increases the amplitude of cardiac K⁺ current (I_K.ACh) through activation of the muscarinic K⁺ (K_ACh) channel, but the amplitude gradually decreases to a quasi-steady-state level within seconds. This phenomenon, known as short-term desensitization, is believed to play a role in cellular adaptation to external input. However, the precise mechanism and physiological role of short-term desensitization is still unclear. In the present review, we introduced our experimental and theoretical studies on the mechanisms underlying short-term desensitization of I_K.ACh. In atrial myocytes, short-term desensitization features the unique dose responses of the transient and quasi-steady state I_K.ACh, effects of ACh preperfusion and recovery from short-term desensitization. In simulation analysis, two conditions are required for the mathematical I_K.ACh model to reconstitute short-term desensitization. The first condition is distinct muscarinic receptors (M₂Rs) with different affinities for ACh, which conferred an I_K.ACh response over a wide range of ACh concentrations. The second condition is 2 distinct K_ACh channels with different affinities for the G-proteinβγsubunit, which contributes to reconstitution of the temporal behavior of I_K.ACh. Under these conditions, the model quantitatively reproduced the unique properties of short-term desensitization observed in experiments. Furthermore, the present model conferred vagal escape on the mathematical action potential models of sinus node cells. Therefore, 2 different populations of K_ACh channels and M₂Rs may be responsible for short-term desensitization and vagal escape at nodal cells.

DOI： 10.5105/jse.35.245

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Other Link： http://search.jamas.or.jp/link/ui/2016139097

Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

The cochlea of the mammalian inner ear contains an endolymph that exhibits an endocochlear potential (EP) of +80 mV with a [K+] of 150 mM. This unusual extracellular solution is maintained by the cochlear lateral wall, a double-layered epithelial-like tissue. Acoustic stimuli allow endolymphatic K+ to enter sensory hair cells and excite them. The positive EP accelerates this K+ influx, thereby sensitizing hearing. K+ exits from hair cells and circulates back to the lateral wall, which unidirectionally transports K+ to the endolymph. In vivo electrophysiological assays demonstrated that the EP stems primarily from two K+ diffusion potentials yielded by [K+] gradients between intracellular and extracellular compartments in the lateral wall. Such gradients seem to be controlled by ion channels and transporters expressed in particular membrane domains of the two layers. Analyses of human deafness genes and genetically modified mice suggested the contribution of these channels and transporters to EP and hearing. A computational model, which reconstitutes unidirectional K+ transport by incorporating channels and transporters in the lateral wall and connects this transport to hair cell transcellular K+ fluxes, simulates the circulation current flowing between the endolymph and the perilymph. In this model, modulation of the circulation current profile accounts for the processes leading to EP loss under pathological conditions. This article not only summarizes the unique physiological and molecular mechanisms underlying homeostasis of the EP and their pathological relevance but also describes the interplay between EP and circulation current.

DOI： 10.1007/s00424-016-1871-0

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

Eukaryotic cells exhibit negative resting membrane potential (RMP) owing to the high K+ permeability of the plasma membrane and the asymmetric [K+] between the extracellular and intracellular compartments. However, cochlear fibrocytes, which comprise the basolateral surface of a multi-layer epithelial-like tissue, exhibit a RMP of +5 to +12 mV in vivo. This positive RMP is critical for the formation of an endocochlear potential (EP) of +80 mV in a K+-rich extracellular fluid, endolymph. The epithelial-like tissue bathes fibrocytes in a regular extracellular fluid, perilymph, and apically faces the endolymph. The EP, which is essential for hearing, represents the potential difference across the tissue. Using in vivo electrophysiological approaches, we describe a potential mechanism underlying the unusual RMP of guinea pig fibrocytes. The RMP was + 9.0 +/- 3.7 mV when fibrocytes were exposed to an artificial control perilymph (n = 28 cochleae). Perilymphatic perfusion of a solution containing low [Na+] (1 mM) markedly hyperpolarized the RMP to -31.1 +/- 11.2 mV (n = 10; p < 0.0001 versus the control, TukeyKramer test after one-way ANOVA). Accordingly, the EP decreased. Little change in RMP was observed when the cells were treated with a high [K+] of 30 mM (+ 10.4 +/- 2.3 mV; n= 7; p = 0.942 versus the control). During the infusion of a low [Cl-] solution (2.4 mM), the RMP moderately hyperpolarized to -0.9 +/- 3.4 mV (n = 5; p < 0.01 versus the control), although the membranes, if governed by Cl-permeability, should be depolarized. These observations imply that the fibrocyte membranes are more permeable to Na+ than K+ and Cl-, and this unique profile and [Na+] gradient across the membranes contribute to the positive RMP.

DOI： 10.1007/s00424-016-1853-2

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER JAPAN KK  

In response to the elevation of extracellular K+ concentration ([K+](out)), astrocytes clear excessive K+ to maintain conditions necessary for neural activity. K+ clearance in astrocytes occurs via two processes: K+ uptake and K+ spatial buffering. High [K+](out) also induces swelling in astrocytes, leading to edema and cell death in the brain. Despite the importance of astrocytic K+ clearance and swelling, the underlying mechanisms remain unclear. Here, we report results from a simulation analysis of astrocytic K+ clearance and swelling. Astrocyte models were constructed by incorporating various mechanisms such as intra/extracellular ion concentrations of Na+, K+, and Cl-, cell volume, and models of Na, K-ATPase, Na-K-Cl cotransporter (NKCC), K-Cl cotransporter, inwardly-rectifying K+ (KIR) channel, passive Cl- current, and aquaporin channel. The simulated response of astrocyte models under the uniform distribution of high [K+](out) revealed significant contributions of NKCC and Na, K-ATPase to increases of intracellular K+ and Cl- concentrations, and swelling. Moreover, we found that, under the non-uniform distribution of high [K+](out), KIR channels localized at synaptic clefts absorbed excess K+ by depolarizing the equivalent potential of K+ (E-K) above membrane potential, while K+ released through perivascular KIR channels was enhanced by hyperpolarizing E-K and depolarizing membrane potential. Further analysis of simulated drug effects revealed that astrocyte swelling was modulated by blocking each of the ion channels and transporters. Our simulation analysis revealed controversial mechanisms of astrocytic K+ clearance and swelling resulting from complex interactions among ion channels and transporters.

DOI： 10.1007/s12576-015-0404-5

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE  

Although anatomical constraints have been shown to be effective for MEG and EEG inverse solutions, there are still no effective physiological constraints. Strength of the current generator is normally described by the moment of an equivalent current dipole Q. This value is quite variable since it depends on size of active tissue. In contrast, the current dipole moment density q, defined as Q per surface area of active cortex, is independent of size of active tissue. Here we studied whether the value of q has a maximum in physiological conditions across brain structures and species. We determined the value due to the primary neuronal current (q(primary)) alone, correcting for distortions due to measurement conditions and secondary current sources at boundaries separating regions of differing electrical conductivities. The values were in the same range for turtle cerebellum(0.56-1.48 nAm/mm(2)), guinea pig hippocampus (0.30-1.34 nAm/mm(2)), and swine neocortex (0.18-1.63 nAm/mm(2)), rat neocortex (similar to 2.2 nAm/mm(2)), monkey neocortex (similar to 0.40 nAm/mm(2)) and human neocortex (0.16- 0.77 nAm/mm(2)). Thus, there appears to be a maximum value across the brain structures and species (1-2 nAm/mm(2)). The empirical values closely matched the theoretical values obtained with our independently validated neural network model (1.6-2.8 nAm/mm(2) for initial spike and 0.7-3.1 nAm/mm(2) for burst), indicating that the apparent invariance is not coincidental. Our model study shows that a single maximum value may exist across a wide range of brain structures and species, varying in neuron density, due to fundamental electrical properties of neurons. The maximum value of qprimary may serve as an effective physiological constraint for MEG/EEG inverse solutions. (C) 2015 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.neuroimage.2015.02.003

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Biophysical Society  

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Language：Japanese   Publisher：日本耳鼻咽喉科学会  

CiNii Books

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATL ACAD SCIENCES  

Sound-evoked mechanical stimuli permit endolymphatic K+ to enter sensory hair cells. This transduction is sensitized by an endocochlear potential (EP) of +80 mV in endolymph. After depolarizing the cells, K+ leaves hair cells in perilymph, and it is then circulated back to endolymph across the lateral cochlear wall. In theory, this process entails a continuous and unidirectional current carried by apical K+ channels and basolateral K+ uptake transporters in both the marginal cell and syncytial layers of the lateral wall. The transporters regulate intracellular and extracellular [K+], allowing the channels to form K+ diffusion potentials across each of the two layers. These diffusion potentials govern the EP. What remains uncertain is whether these transport mechanisms accumulating across diverse cell layers make up a continuous circulation current in the lateral wall and how this current might affect the characteristics of the endolymph. To address this question, we developed an electrophysiological model that incorporates channels and transporters of the lateral wall and channels of hair cells that derive a circulation current. The simulation replicated normal experimental EP values and reproduced experimentally measured changes in the EP and intra-and extracellular [K+] in the lateral wall when different transporters and channels were blocked. The model predicts that, under these different conditions, the circulation current's contribution to the EP arises from different sources. Finally, our model also accurately simulated EP loss in a mouse model of a chloride channelopathy associated with deafness.

DOI： 10.1073/pnas.1120067109

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Japanese Ciruculation Society  

Background: Ventricular tachyarrhythmia is the leading cause of sudden cardiac death, and scroll wave re-entry is known to underlie this condition. Class III antiarrhythmic drugs are commonly used worldwide to treat ventricular tachyarrhythmias
however, these drugs have a proarrhythmic adverse effect and can cause Torsade de Pointes or ventricular fbrillation. Transmural dispersion of repolarization (TDR) has been suggested to be a strong indicator of ventricular tachyarrhythmia induction. However, the role of TDR during sustained scroll wave re-entry is poorly understood. The purpose of the present study was to investigate how TDR affects scroll wave behavior and to provide a novel analysis of the mechanisms that sustain tachyarrhythmias, using computer simulations. Methods and Results: Computer simulations were carried out to quantify the TDR and QT interval under a variety of Iks and Ikr during transmural conduction. Simulated scroll wave re-entries were done under a variety of Iks and Ikr in a ventricular wall slab model, and the scroll wave behavior and the flament dynamics (3-dimensional organizing center) were analyzed. A slight increase in TDR, but not in the QT interval, refected antiarrhythmic properties resulting from the restraint of scroll wave breakup, whereas a marked increase in TDR was proarrhythmic, as a result of scroll wave breakup. Conclusions: The TDR determines the sustainment of ventricular tachyarrhythmias, through control of the scroll wave flament dynamics.

DOI： 10.1253/circj.CJ-10-0071

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Authorship：Lead author   Language：Japanese   Publisher：医学書院  

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：The Royal Society  

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Authorship：Lead author   Language：Japanese   Publishing type：Research paper (scientific journal)   Publisher：日本生体医工学会  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Scoiety  

Inwardly rectifying K(+) (Kir) channels allow K(+) to move more easily into rather than out of the cell. They have diverse physiological functions depending on their type and their location. There are seven Kir channel subfamilies that can be classified into four functional groups: classical Kir channels (Kir2.x) are constitutively active, G protein-gated Kir channels (Kir3.x) are regulated by G protein-coupled receptors, ATP-sensitive K(+) channels (Kir6.x) are tightly linked to cellular metabolism, and K(+) transport channels (Kir1.x, Kir4.x, Kir5.x, and Kir7.x). Inward rectification results from pore block by intracellular substances such as Mg(2+) and polyamines. Kir channel activity can be modulated by ions, phospholipids, and binding proteins. The basic building block of a Kir channel is made up of two transmembrane helices with cytoplasmic NH(2) and COOH termini and an extracellular loop which folds back to form the pore-lining ion selectivity filter. In vivo, functional Kir channels are composed of four such subunits which are either homo- or heterotetramers. Gene targeting and genetic analysis have linked Kir channel dysfunction to diverse pathologies. The crystal structure of different Kir channels is opening the way to understanding the structure-function relationships of this simple but diverse ion channel family.

DOI： 10.1152/physrev.00021.2009

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Language：Japanese   Publisher：The Japanese Society of Electrocardiology  

DOI： 10.5105/jse.29.126

CiNii Books

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Other Link： http://search.jamas.or.jp/link/ui/2009199477

Language：Japanese   Publisher：(一社)日本不整脈心電学会  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier  

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Language：Japanese   Publishing type：Research paper (scientific journal)   Publisher：日本生体医工学会  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer  

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Language：Japanese   Publisher：(一社)日本不整脈心電学会  

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Language：Japanese   Publisher：(一社)日本不整脈心電学会  

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Language：Japanese   Publishing type：Research paper (scientific journal)  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER PHYSIOLOGICAL SOC  

Pharmacological treatment with various antiarrhythmic agents for the termination or prevention of atrial fibrillation (AF) is not yet satisfactory. This is in part because the drugs may not be sufficiently selective for the atrium, and they often cause ventricular arrhythmias. The ultrarapid-delayed rectifying potassium current (I-Kur) is found in the atrium but not in the ventricle, and it has been recognized as a potentially promising target for anti-AF drugs that would be without ventricular proarrhythmia. Several new agents that specifically block I-Kur have been developed. They block I-Kur in a voltage- and time-dependent manner. Here we use mathematical models of normal and electrically remodeled human atrial action potentials to examine the effects of the blockade kinetics of I-Kur on atrial action potential duration (APD). It was found that after AF remodeling, an I-Kur blocker with fast onset can effectively prolong APD at any stimulus frequency, whereas a blocker with slow onset prolongs APD in a frequency- dependent manner only when the recovery is slow. The results suggest that the voltage and time dependence of IKur blockade should be taken into account in the testing of anti-AF drugs. This modeling study suggests that a simple voltage-clamp protocol with a short pulse of similar to 10 ms at 1 Hz may be useful to identify the effective anti-AF drugs among various I-Kur blockers.

DOI： 10.1152/ajpheart.01229.2007

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：PERGAMON-ELSEVIER SCIENCE LTD  

The inactivation of the L-type Ca2+ current is composed of voltage-dependent and calcium -dependent mechanisms. The relative contribution of these processes is still under dispute and the idea that the voltage-dependent inactivation could be subject to further modulation by other physiological processes had been ignored. This study sought to model physiological modulation of inactivation of the current in cardiac ventricular myocytes, based upon the recent detailed experimental data that separated total and voltage-dependent inactivation (VDI) by replacing extracellular Ca2+ with Mg2+ and monitoring L-type Ca2+ channel behaviour by outward K+ current flowing through the channel in the absence of inward current flow. Calcium -dependent inactivation (CDI) was based upon Ca2+ influx and formulated from data that was recorded during beta-adrenergic stimulation of the myocytes. Ca2+ influx and its competition with non-selective monovalent cation permeation were also incorporated into channel permeation in the model. The constructed model could closely reproduce the experimental Ba2+ and Ca2+ current results under basal condition where no beta-stimulation was added after a slight reduction of the development of fast voltage-dependent inactivation with depolarization. The model also predicted that under beta-adrenereic stimulation voltage-dependent inactivation is lost and calcium-dependent inactivation largely compensates it. The developed model thus will be useful to estimate the respective roles of VDI and CDI of L-type Ca2+ channels in various physiological and pathological conditions of the heart which would otherwise be difficult to show experimentally. (C) 2007 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.pbiomolbio.2007.07.002

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE PHARMACOLOGICAL SOC  

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：PHYSIOLOGICAL SOCIETY OF JAPAN  

Ca²⁺ dynamics underlying cardiac excitation-contraction coupling are essential for heart functions. In this study, we constructed microstructure-based models of Ca²⁺ dynamics to simulate Ca²⁺ influx through individual L-type calcium channels (LCCs), an effective Ca²⁺ diffusion within the cytoplasmic space and in the dyadic space, and the experimentally observed calcium-dependent inactivation (CDI) of the LCCs induced by local and global Ca²⁺ sensing. The models consisted of LCCs with distal and proximal Ca²⁺ (Calmodulin-Ca²⁺ complex) binding sites. In one model, the intracellular space was organelle-free cytoplasmic space, and the other was with a dyadic space including sarcoplasmic reticulum membrane. The Ca²⁺ dynamics and CDI of the LCCs in the model with and without the dyadic space were then simulated using the Monte Carlo method. We first showed that an appropriate set of parameter values of the models with effectively extra-slow Ca²⁺ diffusion enabled the models to reproduce major features of the CDI process induced by the local and global sensing of Ca²⁺ near LCCs as measured with single and two spatially separated LCCs by Imredy and Yue (Neuron. 1992;9:197-207). The effective slow Ca²⁺ diffusion might be due to association and dissociation of Ca²⁺ and Calmodulin (CaM). We then examined how the local and global CDIs were affected by the presence of the dyadic space. The results suggested that in microstructure modeling of Ca²⁺ dynamics in cardiac myocytes, the effective Ca²⁺ diffusion under CaM-Ca²⁺ interaction, the nanodomain structure of LCCs for detailed CDI, and the geometry of subcellular space for modeling dyadic space should be considered.<br>

DOI： 10.2170/physiolsci.RP013208

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Authorship：Lead author   Language：English   Publishing type：Part of collection (book)   Publisher：Springer London  

Antiarrhythmic drugs have been used as an effective measure to treat or prevent tachyarrhythmias including ventricular tachycardia and fibrillation in clinics for a long time. Arrhythmias refer to changes from the normal sequence of electrical impulses and conduction, causing abnormal heart rhythms. They can be classified into two categories: bradyarrhythmias and tachyarrhythmias. Both can make the heart pump less effectively and, more seriously, cause sudden death. Possible treatments include electrical defibrillation, radio frequency ablation, implantable cardioverter defibrillators, artificial pacemakers, and medication. All these are used to prevent or terminate arrhythmias. Among them, arrhythmia medication is a nonsurgical and effective treatment and its major target has been tachyarrhythmias, mainly in the ventricle, including ventricular tachycardia and fibrillation. Of course, recently treatment of atrial tachyarrhythmias such as atrial fibrillation is also one of the major interests. However, its application may cause serious adverse effects.1 Since usage of antiarrhythmic drugs tended to rely on clinicians' experience and to be based on clinical practice, the effects of antiarrhythmic drugs had been understood empirically. Accumulated studies on the mechanism of antiarrhythmic agents, however, have provided much basic understanding of drug action, especially on the electrophysiological properties of cardiac excitation. This will not only help clinicians to select proper antiarrhythmic drugs, but will also help in the development of new antiarrhythmic drugs. © 2008 Springer-Verlag London Limited.

DOI： 10.1007/978-1-84628-854-8_7

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Scoiety  

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：The Physiological Society  

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：CAMBRIDGE UNIV PRESS  

A mathematical model was used to analyse the contributions of different types of ionic currents in the pyramidal cells of longitudinal CA3 slices to the magnetic fields and field potentials generated by this preparation. Murakami et al. recently showed that a model based on the work of Traub et al. provides a quantitatively accurate account of the basic features of three types of empirical data (magnetic fields outside the slice, extracellular field potentials within the slice and intracellular potentials within the pyramidal neurons) elicited by stimulations of the soma and apical dendrites. This model was used in the present study to compute the net current dipole moment (Q) due to each of the different voltage- and ligand-gated channels in the cells in the presence of fast GABA(A) inhibition. These values of Q are proportional to the magnetic field and electrical potential far away from the slice. The intrinsic conductances were found to be more important than the synaptic conductances in determining the shape and magnitude of Q. Among the intrinsic conductances, the sodium (g(Na)) and delayed-rectifier potassium (g(K(DR))) channels were found to produce sharp spikes. The high-threshold calcium channel (g(Ca)) and C-type potassium channel (g,(c)) primarily determined the overall current waveforms. The roles Of g(Ca) and g(K(C)) were independent of small perturbations in these channel densities in the apical and basal dendrites. A combination of g(Na), g(K(DR)), g(Ca), and g(K(C)) accounted for most of the evoked responses, except for later slow components, which were primarily due to synaptic channels.

DOI： 10.1113/jphysiol.2003.051144

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

This study examined whether evoked magnetic fields and intra- and extracellular potentials from longitudinal CA3 slices of guinea-pig can be interpreted within a single theoretical framework that incorporates ligand- and voltage-sensitive conductances in the dendrites and soma of the pyramidal cells. The 1991 CA3 mathematical model of R. D. Traub is modified to take into account the asymmetric branching patterns of the apical and basal dendrites of the pyramidal cells. The revised model accounts for the magnitude and waveform of the bi- and triphasic magnetic fields evoked by somatic and apical stimulations, respectively, in the slice in the absence of fast inhibition (blocked by 0.1 mm picrotoxin). The revised model also accounts for selective effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), which block the potassium channels of A and C type, respectively, on the slow wave of the magnetic fields. Furthermore, the model correctly predicts the laminar profiles of field potential as well as intracellular potentials in the pyramidal cells produced by two classes of cells - those directly activated and those indirectly (synaptically) activated by the applied external stimulus. The intracellular potentials in this validated model reveal that the spikes and slow waves of the magnetic fields are generated in or near the soma and apical dendrites, respectively. These results demonstrate that a single theoretical framework couched within the modern concepts of cellular physiology provides a unified account of magnetic fields outside the slice, extracellular potentials within the slice and intracellular potentials of the pyramidal cells for CA3.

DOI： 10.1113/jphysiol.2002.027094

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