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TY - JOUR. T1 - Voltage-dependent sodium channel function is regulated through membrane mechanics. AU - Shcherbatko, Anatoly. AU - Ono, Fumihito. AU - Mandel, Gail. AU - Brehm, Paul. PY - 1999/10. Y1 - 1999/10. N2 - Cut-open recordings from Xenopus oocytes expressing either nerve (PN1) or skeletal muscle (SkM1) Na+ channel α subunits revealed slow inactivation onset and recovery kinetics of inward current. In contrast, recordings using the macropatch configuration resulted in an immediate negative shift in the voltage-dependence of inactivation and activation, as well as time-dependent shifts in kinetics when compared to cut-open recordings. Specifically, a slow transition from predominantly slow onset and recovery to exclusively fast onset and fast recovery from inactivation occurred. The shift to fast inactivation was accelerated by patch excision and by agents that disrupted microtubule formation. Application of positive pressure to cell-attached macropatch electrodes prevented the shift in ...
Action potential generation in excitable cells such as myocytes and neurons critically depends on voltage-gated sodium channels. In mammals, sodium channels exist as macromolecular complexes that include a pore-forming alpha subunit and 1 or more modulatory beta subunits. Although alpha subunit genes have been cloned from diverse metazoans including flies, jellyfish, and humans, beta subunits have not previously been identified in any non-mammalian species. To gain further insight into the evolution of electrical signaling in vertebrates, we investigated beta subunit genes in the teleost Danio rerio (zebrafish). We identified and cloned single zebrafish gene homologs for beta1-beta3 (zbeta1-zbeta3) and duplicate genes for beta4 (zbeta4.1, zbeta4.2). Sodium channel beta subunit loci are similarly organized in fish and mammalian genomes. Unlike their mammalian counterparts, zbeta1 and zbeta2 subunit genes display extensive alternative splicing. Zebrafish beta subunit genes and their splice variants are
Previously cloned voltage-dependent sodium channels exhibit a high degree of homology to one another and appear to comprise a single multigene family. We have now isolated and characterized cDNAs from both human adult heart and fetal skeletal muscle that encode a sodium channel alpha subunit that exhibits only moderate primary structure identity with other sodium channels and is prominently expressed in both heart and uterus. The approximately 7.2-kilobase cDNA sequence, designated hNav2.1, predicts a 1682-amino acid protein that bears 52%, 49%, and 46% overall identity with sodium channels cloned from rat brain, skeletal muscle, and heart, respectively. Positively charged S4 segments are present in hNav2.1, but there are fewer basic residues in repeat domains 1, 3, and 4 than in other cloned sodium channels. The cloning of hNav2.1 provides evidence for greater evolutionary divergence among voltage-dependent sodium channels and suggests that other sodium channel gene subfamilies may exist. The ...
Navα1.2, also known as the sodium channel, voltage-gated, type II, alpha subunit is a protein that in humans is encoded by the SCN2A gene. Functional sodium channels contain an ion conductive alpha subunit and one or more regulatory beta subunits. Sodium channels which contain the Navα1.2 subunit are called Nav1.2 channels. Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with four domains including 24 transmembrane segments and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family. It is heterogeneously expressed in the brain, and mutations in this gene have been linked to several seizure disorders. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined. Mutations in this ...
Voltage-gated ion channels allow electrically excitable cells to generate and propagate action potentials and therefore are crucial for nerve and muscle function. Sodium channels play a special role by mediating rapid depolarization, which constitutes the rising phase of the action potential and in turn activates voltage-gated calcium and potassium channels. Voltage-gated sodium channels represent a multigene family. Nine sodium channel subtypes have been cloned and functionally expressed to date. [Clare, J. J., Tate, S. N., Nobbs, M. & Romanes, M. A. Voltage-gated sodium channels as therapeutic targets. Drug Discovery Today 5, 506-520 (2000)]. They are differentially expressed throughout muscle and nerve tissues and show distinct biophysical properties. All voltage-gated sodium channels are characterized by a high degree of selectivity for sodium over other ions and by their voltage-dependent gating. [Catterall, W. A. Structure and function of voltage-gated sodium and calcium channels. Current ...
Background: Mutations in voltage gated brain sodium channel Nav1.1 have been linked to many disorders, including Generalized Epilepsy with Febrile Seizures Plus (GEFS+) and Severe Myoclonic Epilepsy of Infancy (SMEI). Recent studies have identified TTX- sensitive Nav1.1 brain sodium channels in the SA node and ventricular T-tubules of the heart, though their role in cardiac function is still controversial. We tested the functional significance of Nav1.1 sodium channels in the heart by creating a novel knock-in of human epilepsy GEFS+ mutation SCN1A-R1648H at the Scn1a locus of a C57BL/6J X 129 mouse.. Method: In vivo 2-D echocardiography was performed on 2 week old (juvenile) and 8 week old (adult) wild-type and heterozygote (Scn1aRH/+) mice after extracardiac neuronal block through intraperitoneal injections of atropine and propranolol (2.5mg/kg each). Calcium and contractility studies on adult ventricular cardiomyocytes isolated from the wild type and Scn1aRH/+ mice paced at 0.5Hz were ...
Voltage-dependent sodium channels are heteromeric complexes that regulate sodium exchange between intracellular and extracellular spaces and are essential for the generation and propagation of action potentials in muscle cells and neurons. Each sodium channel is composed of a large pore-forming, glycosylated alpha subunit and two smaller beta subunits. This gene encodes a sodium channel alpha subunit, which has four homologous domains, each of which contains six transmembrane regions. Allelic variants of this gene are associated with generalized epilepsy with febrile seizures and epileptic encephalopathy. Alternative splicing results in multiple transcript variants. The RefSeq Project has decided to create four representative RefSeq records. Three of the transcript variants are supported by experimental evidence and the fourth contains alternate 5 untranslated exons, the exact combination of which have not been experimentally confirmed for the full-length transcript. [provided by RefSeq, Oct 2015]
Fingerprint Dive into the research topics of CAP-1A is a novel linker that binds clathrin and the voltage-gated sodium channel Na,sub,v,/sub,1.8. Together they form a unique fingerprint. ...
TY - JOUR. T1 - Stimulatory action of telmisartan, an antagonist of angiotensin II receptor, on voltage-gated Na + current. T2 - Experimental and theoretical studies. AU - Chang, Tzu Tung. AU - Yang, Chia Jung. AU - Lee, Yu Chi. AU - Wu, Sheng-Nan. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Telmisartan (Tel) is recognized as a non-peptide blocker of AT1R. Whether this agent has any direct effects on ion currents remains unexplored. In whole-cell current recordings, addition of Tel increased the peak amplitude of voltage-gated Na + (Na V ) current (I Na ) accompanied by the increased time constant of I Na inactivation in differentiated NSC-34 motor neuron-like cells. Tel-stimulated INa in these cells is unlinked to either blockade of AT1R or activation of peroxisome proliferator-activated receptor gamma (PPAR-γ). In order to explore how this compound affects the amplitude and kinetics of I Na in neurons, a Hodgkin-Huxley-based (HH-based) model designed to mimic effect of Tel on the functional activities ...
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TY - JOUR. T1 - Molecular motions of the outer ring of charge of the sodium channel. T2 - Do they couple to slow inactivation?. AU - Xiong, Wei. AU - Li, Ronald A.. AU - Tian, Yanli. AU - Tomaselli, Gordon F.. PY - 2003/9/1. Y1 - 2003/9/1. N2 - In contrast to fast inactivation, the molecular basis of sodium (Na) channel slow inactivation is poorly understood. It has been suggested that structural rearrangements in the outer pore mediate slow inactivation of Na channels similar to C-type inactivation in potassium (K) channels. We probed the role of the outer ring of charge in inactivation gating by paired cysteine mutagenesis in the rat skeletal muscle Na channel (rNav1.4). The outer charged ring residues were substituted with cysteine, paired with cysteine mutants at other positions in the external pore, and coexpressed with rat brain β 1 in Xenopus oocytes. Dithiolthreitol (DTT) markedly increased the current in E403C+E758C double mutant, indicating the spontaneous formation of a disulfide ...
Authors: Larry Baum, Batoul Sadat Haerian, Ho-Keung Ng, Virginia CN Wong, Ping Wing Ng, Colin HT Lui, Ngai Chuen Sin, Chunbo Zhang, Brian Tomlinson, Gary Wing-Kin Wong, Hui Jan Tan, Azman Ali Raymond, Zahurin Mohamed, Patrick Kwan
TY - JOUR. T1 - Sodium channels and pain. AU - Waxman, S. G.. AU - Dib-Hajj, S.. AU - Cummins, T. R.. AU - Black, J. A.. PY - 1999/7/6. Y1 - 1999/7/6. N2 - Although it is well established that hyperexcitability and/or increased baseline sensitivity of primary sensory neurons can lead to abnormal burst activity associated with pain, the underlying molecular mechanisms are not fully understood. Early studies demonstrated that, after injury to their axons, neurons can display changes in excitability, suggesting increased sodium channel expression, and, in fact, abnormal sodium channel accumulation has been observed at the lips of injured axons. We have used an ensemble of molecular, electrophysiological, and pharmacological techniques to ask: what types of sodium channels underlie hyperexcitability of primary sensory neurons after injury? Our studies demonstrate that multiple sodium channels, with distinct electrophysiological properties, are encoded by distinct mRNAs within small dorsal root ...
Background- We and others have reported mutations in the cardiac predominant sodium channel gene SCN5A in patients with atrial fibrillation (AF). We also have reported that SCN1B is associated with Brugada syndrome and isolated cardiac conduction disease. We tested the hypothesis that mutations in the 4 sodium channel β-subunit genes SCN1B-SCN4B contribute to AF susceptibility.. Methods and Results- Screening for mutations in the 4 β-subunit genes was performed in 480 patients with AF (118 patients with lone AF and 362 patients with AF and cardiovascular disease) and 548 control subjects (188 ethnically defined anonymized subjects and 360 subjects without AF). The effects of mutant β-subunits on SCN5A mediated currents were studied using electrophysiological studies. We identified 2 nonsynonymous variants in SCN1B (resulting in R85H, D153N) and 2 in SCN2B (R28Q, R28W) in patients with AF. These occur at residues highly conserved across mammals and were absent in control subjects. In 3 of 4 ...
The overall aim of this PhD was to improve our understanding, including the clinical potential, of neonatal Nav1.5 (nNav1.5) expression in human metastatic breast cancer. Mainly, the strongly metastatic MDA-MB-231 cells were used throughout the studies. The specific aims were threefold, as follows: 1) To test the effects of several types of voltage-gated sodium channel (VGSC) blocker on nNav1.5 mRNA and protein expression and metastatic cell behaviours (MCBs); (2) to determine the effects of hypoxia on the drug treatments and MCBs; and (3) to elucidate a possible association of carbonic anhydrase-9 (CA9) and nNav1.5 expression/activity. There are three main Results chapters. Results-1 demonstrates the effects of the drugs on MCBs of MDA-MB-231 cells under normal oxygen level (normoxia). Two classes of blocker were used: a) Local anaesthetics (lidocaine and procaine) and (b) blockers of persistent current (INaP) (ranolazine and riluzole). In addition, a specific VGSC blocker, tetrodotoxin (TTX), ...
Atherton, J. F., Gillies, A. J., Corbett, A. M., & Arbuthnott, G. W. (1998). The Relationship Between Voltage-Gated Sodium Channel Inactivation Firing Frequency in the Subthalamic Nucleus Projection Neuron. European Journal of Neuroscience, 10 (Supplement 10), 300 ...
Voltage-gated sodium channels are important targets for the development of pharmaceutical drugs, because mutations in different human sodium channel isoforms have causal relationships with a range of neurological and cardiovascular diseases. In this study, functional electrophysiological studies show that the prokaryotic sodium channel from Magnetococcus marinus (NavMs) binds and is inhibited by eukaryotic sodium channel blockers in a manner similar to the human Nav1.1 channel, despite millions of years of divergent evolution between the two types of channels. Crystal complexes of the NavMs pore with several brominated blocker compounds depict a common antagonist binding site in the cavity, adjacent to lipid-facing fenestrations proposed to be the portals for drug entry. In silico docking studies indicate the full extent of the blocker binding site, and electrophysiology studies of NavMs channels with mutations at adjacent residues validate the location. These results suggest that the NavMs ...
Batrachotoxin (BTX), from South American frogs of the genusPhyllobates, irreversibly activates voltage-gated sodium channels. Previous work demonstrated that a phenylalanine residue approximately halfway through pore-lining transmembrane segment IVS6 is a critical determinant of channel sensitivity to BTX. In this study, we introduced a series of mutations at this site in the Nav1.3 sodium channel, expressed wild-type and mutant channels inXenopus laevis oocytes, and examined their sensitivity to BTX using voltage clamp recording. We found that substitution of either alanine or isoleucine strongly reduced channel sensitivity to toxin, whereas cysteine, tyrosine, or tryptophan decreased toxin action only modestly. These data suggest an electrostatic ligand-receptor interaction at this site, possibly involving a charged tertiary amine on BTX. We then used a mutant channel (mutant F1710C) with intermediate toxin sensitivity to examine the properties of the toxin-receptor reaction in more detail. In ...
Modulates channel gating kinetics. Causes unique persistent sodium currents. Inactivates the sodium channel opening more slowly than the subunit beta-1. Its association with NFASC may target the sodium channels to the nodes of Ranvier of developing axons and retain these channels at the nodes in mature myelinated axons (By similarity).
Lubeluzole is widely reported as a multitarget drug acting at least on voltage-gated calcium and sodium channels. There are, however, only a very few studies reporting direct demonstration of sodium channel blockade by lubeluzole in neuronal and cardiac cells (Osikowska-Evers et al., 1995; Le Grand et al., 2003). The more complete study by Le Grand et al., (2003) described the block of sodium channels in single guinea pig ventricular myocytes. It was shown that lubeluzole produces a concentration-dependent tonic and use-dependent block of cardiac sodium channels in a manner similar to that of class I antiarrhythmic drugs, suggesting a greater affinity for inactivated than for resting channels. In the present study, we observed a similar local anesthetic-like effect of lubeluzole on human skeletal muscle sodium channels, and definitely demonstrated that the drug is a very potent blocker of inactivated sodium channels compared with resting channels. The IC50 values calculated for skeletal muscle ...
Voltage-gated sodium channels play a critical role in the generation and conduction of action potentials - so important for electrical signalling by most excitable cells. Sodium channels are integral membrane proteins and are comprised of a large α subunit, which forms the voltage-sensitive and ion-selective pore, and smaller auxiliary β subunit(s) that can modulate the kinetics and voltage dependence of channel gating. Till 2007, 9 isoforms of the sodium-channel α subunit (Nav1.1- Nav1.9), each with a unique central and peripheral nervous system distribution had been identified. 4 closely related sodium channels (Nav 1.1, -1.2, -1.3, and -1.7) are encoded by a set of 4 genes (SCN1A, SCN2A, SCN3A, and SCN9A, respectively) located within a cluster on chromosome 2q24.3. Mutations in the genes encoding Nav1.1, -1.2, and -1.3 are responsible for a group of epilepsy syndromes with overlapping clinical characteristics but divergent clinical severity, mutation in the gene encoding Nav1.7 has a ...
Definition of sodium channel blocking agent in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is sodium channel blocking agent? Meaning of sodium channel blocking agent as a legal term. What does sodium channel blocking agent mean in law?
Voltage-gated sodium channels (NaV) are plasma membrane ion channels that physiological activity is critical for cellular electricity and the functioning of cells characterized as being
TY - JOUR. T1 - Ca 2+ -dependent regulation of sodium channels Na V 1.4 and Na V 1.5 is controlled by the post-IQ motif AU - Yoder, Jesse B.. AU - Ben-Johny, Manu. AU - Farinelli, Federica. AU - Srinivasan, Lakshmi. AU - Shoemaker, Sophie R.. AU - Tomaselli, Gordon F.. AU - Gabelli, Sandra B.. AU - Amzel, L. Mario. PY - 2019/12/1. Y1 - 2019/12/1. N2 - Skeletal muscle voltage-gated Na + channel (Na V 1.4) activity is subject to calmodulin (CaM) mediated Ca 2+ -dependent inactivation; no such inactivation is observed in the cardiac Na + channel (Na V 1.5). Taken together, the crystal structures of the Na V 1.4 C-terminal domain relevant complexes and thermodynamic binding data presented here provide a rationale for this isoform difference. A Ca 2+ -dependent CaM N-lobe binding site previously identified in Na V 1.5 is not present in Na V 1.4 allowing the N-lobe to signal other regions of the Na V 1.4 channel. Consistent with this mechanism, removing this binding site in Na V 1.5 unveils robust Ca ...
Long QT syndrome (LQT) is an inherited cardiac disorder that causes syncope, seizures and sudden death from ventricular tachyarrhythmias. We used single-strand conformation polymorphism (SSCP) and DNA sequence analyses to identify mutations in the cardiac sodium channel gene, SCN5A, in affected members of four LQT families. These mutations include two identical intragenic deletions and two missense mutations. These data suggest that SCN5A mutations cause LQT. The location and character of these mutations suggest that this form of LQT results from a delay in cardiac sodium channel fast inactivation or altered voltage-dependence of inactivation. ...
Arrhythmias arise from breakdown of orderly action potential (AP) activation, propagation and recovery driven by interactive opening and closing of successive voltage-gated ion channels, in which one or more Na+ current components play critical parts. Early peak, Na+ currents (I Na) reflecting channel activation drive the AP upstroke central to cellular activation and its propagation. Sustained late Na+ currents (I Na-L) include contributions from a component with a delayed inactivation timecourse influencing AP duration (APD) and refractoriness, potentially causing pro-arrhythmic phenotypes. The magnitude of I Na-L can be analysed through overlaps or otherwise in the overall voltage dependences of the steady-state properties and kinetics of activation and inactivation of the Na+ conductance. This was useful in analysing repetitive firing associated with paramyotonia congenita in skeletal muscle. Similarly, genetic cardiac Na+ channel abnormalities increasing I Na-L are implicated in triggering
Sodium channel protein type 7 subunit alpha is a protein that in humans is encoded by the SCN7A gene on the chromosome specifically located at 2q21-23 chromosome site. This is one of 10 Sodium channel types, and is expressed in the heart, the uterus and in glial cells. Its sequence identity is 48, and it is the only sodium channel known to be completely un-blockable by TTX (tetrodotoxin). Sodium channel Scn7a is the name of the gene that encodes to a membrane protein, in particular a Sodium Channel Nax (also known as NaG, Nav2.1, etc.) It belongs to a family of Sodium Channel known as Voltage-Gated, but is not activated by changes in the membranes voltage, as happen usually in the members of this family (Nav1.1 to Nav1.9); it activates by changes in the extracellular concentration of sodium [~150 mM]. GRCh38: Ensembl release 89: ENSG00000136546 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000034810 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Plummer NW, ...
Background- We and others have reported mutations in the cardiac predominant sodium channel gene SCN5A in patients with atrial fibrillation (AF). We also have reported that SCN1B is associated with Brugada syndrome and isolated cardiac conduction disease. We tested the hypothesis that mutations in the 4 sodium channel β-subunit genes SCN1B-SCN4B contribute to AF susceptibility.. Methods and Results- Screening for mutations in the 4 β-subunit genes was performed in 480 patients with AF (118 patients with lone AF and 362 patients with AF and cardiovascular disease) and 548 control subjects (188 ethnically defined anonymized subjects and 360 subjects without AF). The effects of mutant β-subunits on SCN5A mediated currents were studied using electrophysiological studies. We identified 2 nonsynonymous variants in SCN1B (resulting in R85H, D153N) and 2 in SCN2B (R28Q, R28W) in patients with AF. These occur at residues highly conserved across mammals and were absent in control subjects. In 3 of 4 ...
Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient.
TY - JOUR. T1 - A gating hinge in Na+ channels. T2 - A molecular switch for electrical signaling. AU - Zhao, Yong. AU - Yarov-Yarovoy, Vladimir. AU - Scheuer, Todd. AU - Catterall, William A.. PY - 2004/3/25. Y1 - 2004/3/25. N2 - Voltage-gated sodium channels are members of a large family with similar pore structures. The mechanism of opening and closing is unknown, but structural studies suggest gating via bending of the inner pore helix at a glycine hinge. Here we provide functional evidence for this gating model for the bacterial sodium channel NaChBac. Mutation of glycine 219 to proline, which would strongly favor bending of the α helix, greatly enhances activation by shifting its voltage dependence -51 mV and slowing deactivation by 2000-fold. The mutation also slows voltage-dependent inactivation by 1200-fold. The effects are specific because substitutions of proline at neighboring positions and substitutions of other amino acids at position 219 have much smaller functional effects. Our ...
Cells were dispersed from the brains of the triclad flatworm Bdelloura candida and maintained in primary culture for up to 2 weeks. Cultured cells assumed a variety of morphologies consistent with those of neurones in vivo. Whole-cell voltage-clamp recordings from cultured cells revealed that these cells possess a variety of ionic currents, including a fast transient sodium current, a calcium current and several potassium currents. The sodium current does not inactivate completely but instead decays to a steady-state component which has the same physiology and pharmacology as the fast transient component, suggesting that the two components are carried by the same population of channels. The physiology and pharmacology of these various currents were not remarkable save for the fact that, contrary to earlier reports, all sodium currents examined were sensitive to tetrodotoxin (TTX). These animals are, therefore, the lowest animals known to possess TTX-sensitive sodium currents and, as such, ...
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Voltage-gated Na+ channels (VGSCs) are heteromeric protein complexes containing pore-forming ? subunits together with non-pore-forming ? subunits. There are nine ? subunits, Nav1.1-Nav1.9, and four ? subunits, ?1-?4. The ? subunits are multifunctional, modulating channel activity, cell surface expression, and are members of the immunoglobulin superfamily of cell adhesion molecules. VGSCs are classically responsible for action potential initiation and conduction in electrically excitable cells, including neurons and muscle cells. In addition, through the ?1 subunit, VGSCs regulate neurite outgrowth and pathfinding in the developing central nervous system. Reciprocal signalling through Nav1.6 and ?1 collectively regulates Na+ current, electrical excitability and neurite outgrowth in cerebellar granule neurons. Thus, ? and ? subunits may have diverse interacting roles dependent on cell/tissue type. VGSCs are also expressed in non-excitable cells, including cells derived from a number of types of cancer. In
In experimental studies, mostly done in laboratory animals, researchers have reported that n-3 PUFAs have several potential anti-arrhythmic effects40, 41-most notably a direct effect on cardiac ion channels. Initial data37 from single-cell experiments with isolated cardiomyocytes showed that acute application of purified n-3 PUFAs had a profound inhibitory effect on sodium channels, reducing the peak sodium current by more than 50% and shifting the steady-state inactivation towards negative potentials, thus reducing excitability. This finding was supported by other similar studies,38, 39 leading to the hypothesis that n-3 PUFAs exert their predominant anti-arrhythmic effect by their inhibitory action on sodium channels. However, when cardiac cells with high membrane incorporation of n-3 PUFA, which was obtained from animals fed a diet fortified with fish oil, were studied, this effect was not consistently reported. Further studies in laboratory animals revealed that n-3 PUFAs have a diverse ...
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This paper shows that persistent sodium current critically contributes to the subthreshold nonlinear dynamics of CA1 pyramidal neurons and promotes rapidly reversible conversion between place-cell and silent-cell in the hippocampus. A simple model built with realistic axo-somatic voltage-gated sodium channels in CA1 (Carter et al., 2012; Neuron 75, 1081-1093) demonstrates that the biophysics of persistent sodium current is sufficient to explain the synaptic amplification effects. A full model built previously (Grienberger et al., 2017; Nature Neuroscience, 20(3): 417-426) with detailed morphology, ion channel types and biophysical properties of CA1 place cells naturally reproduces the steep voltage dependence of synaptic responses ...
The PUFAs act by stabilizing electrically every cardiac myocyte by modulating conductance of ion channels in the sarcolemma, particularly the fast, voltage-dependent sodium current and the L-type calcium currents, though other ion currents are also affected. Work in progress suggests that the primary site of action of the PUFAs may be on the phospholipid bilayer of the heart cells in the microdomains through which the ion channels penetrate the membrane bilayer in juxtaposition with the ion channels rather than directly on the channel protein itself ...
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A cross-section of an axon, with an action potential (AP) moving from left to right. The AP has not yet reached point 4; the membrane there is still at rest. At point 3, positive sodium ions are moving in from the adjacent region, depolarizing the region; the sodium channels are about to open. Point 2 is at the peak of the AP; the sodium channels are open and ions are flowing into the axon. The AP has passed by point 1; the sodium channels are inactivated, and the membrane is hyperpolarized ...
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In the present work, we improve this model neuron by including morphological details. We take the morphological information from identified larval aCC abdominal dorsomedial motoneurons, which innervate the dorsal muscles [4]. A two-compartment version of the model is used to assess effects of changing sodium channel properties. This neuron model allows investigating the effect of sodium channel splice variants by varying half-activation and inactivation voltages and ratio of a persistent component to mimic changes observed in sodium channel current properties in seizure mutants. We further analyze the effect that changes in synaptic input observed in seizure mutants have on the output neuronal activity. ...
Some diseases, such as familial Alzheimers disease (FAD), arise from a mutation in a single gene. In sporadic AD, however, complex interactions among multiple genes underlie the phenotype, and under these circumstances genetic background may strongly influence the manifestation or progression of the disease in ways that largely still stump scientists. A case in point is the mouse sodium channel modifier 1 (SCNM1), a gene that can turn a chronic disorder into a lethal disease.. In the current Science, Miriam Meisler and colleagues at the University of Michigan, Ann Arbor, characterize the SCNM1 mutation, which is found in C57 black 6 (C57BL/6) mice and other closely related strains. In the C57BL/6 background, a mutation in the sodium channel gene 8a (Scn8a) is lethal, and pups die after a month. In the absence of the SCNM1 mutation, however, as in C3H mice, the sodium channel mutation leads to a milder phenotype where the animals live for years, albeit with a chronic movement disorder.. First ...
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Alternative splicing is a post-transcriptional mechanism that can substantially change the pattern of gene expression. Up to 95% of human genes have multi-exon alternative spliced forms, suggesting that alternative splicing is one of the most significant components of the functional complexity of the human genome. Nevertheless, alternative splicing regulation has received comparatively little attention in the study of cardiac diseases. When investigating SCN5A splicing abnormalities in heart failure, we found 47 of 181 known splicing regulators were upregulated in HF when compared to controls, which indicate that splicing regulation may play a key role in heart failure. Our results shows that AngII and hypoxia, signals common to HF, result in increased LUC7L3 and RBM25 splicing regulators, increased binding of RBM25 to SCN5A mRNA, increased SCN5A splice variant abundances, decreased full-length SCN5A mRNA and protein, and decreased Na+ current. These observations could shed light on a mechanism ...
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Eight state kinetic sodium channel gating scheme : Modified from k3st.mod, chapter 9.9 (example 9.7) : of the NEURON book : 12 August 2008, Christoph Schmidt-Hieber : : accompanies the publication: : Schmidt-Hieber C, Bischofberger J. (2010) : Fast sodium channel gating supports localized and efficient : axonal action potential initiation. : J Neurosci 30:10233-42 NEURON { SUFFIX na USEION na READ ena WRITE ina GLOBAL vShift, vShift_inact, maxrate RANGE vShift_inact_local RANGE gna, gbar, ina_ina RANGE a1_0, a1_1, b1_0, b1_1, a2_0, a2_1 RANGE b2_0, b2_1, a3_0, a3_1, b3_0, b3_1 RANGE bh_0, bh_1, bh_2, ah_0, ah_1, ah_2 } UNITS { (mV) = (millivolt) } : initialize parameters PARAMETER { : gbar = 33 (millimho/cm2) gbar = 1000 (pS/um2) a1_0 = 4.584982656184167e+01 (/ms) a1_1 = 2.393541665657613e-02 (/mV) b1_0 = 1.440952344322651e-02 (/ms) b1_1 = 8.847609128769419e-02 (/mV) a2_0 = 1.980838207143563e+01 (/ms) a2_1 = 2.217709530008501e-02 (/mV) b2_0 = 5.650174488683913e-01 (/ms) b2_1 = ...
Edited by H. Ronald Kaback, University of California, Los Angeles, CA, and approved June 8, 2004 (received for review April 15, 2004) ArticleFigures SIInfo Stratagene). CHO-K1 cells were grown in DMDM (Invitrogen) supplemented with 10% FBS