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Journal articles on the topic 'Sodium channels'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Sula, Altin, and B. A. Wallace. "Interpreting the functional role of a novel interaction motif in prokaryotic sodium channels." Journal of General Physiology 149, no. 6 (2017): 613–22. http://dx.doi.org/10.1085/jgp.201611740.

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Voltage-gated sodium channels enable the translocation of sodium ions across cell membranes and play crucial roles in electrical signaling by initiating the action potential. In humans, mutations in sodium channels give rise to several neurological and cardiovascular diseases, and hence they are targets for pharmaceutical drug developments. Prokaryotic sodium channel crystal structures have provided detailed views of sodium channels, which by homology have suggested potentially important functionally related structural features in human sodium channels. A new crystal structure of a full-length

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2

Warmke, Jeffrey W., Robert A. G. Reenan, Peiyi Wang, et al. "Functional Expression of Drosophila para Sodium Channels." Journal of General Physiology 110, no. 2 (1997): 119–33. http://dx.doi.org/10.1085/jgp.110.2.119.

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The Drosophila para sodium channel α subunit was expressed in Xenopus oocytes alone and in combination with tipE, a putative Drosophila sodium channel accessory subunit. Coexpression of tipE with para results in elevated levels of sodium currents and accelerated current decay. Para/TipE sodium channels have biophysical and pharmacological properties similar to those of native channels. However, the pharmacology of these channels differs from that of vertebrate sodium channels: (a) toxin II from Anemonia sulcata, which slows inactivation, binds to Para and some mammalian sodium channels with si

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3

Duch, D. S., E. Recio-Pinto, C. Frenkel, S. R. Levinson, and B. W. Urban. "Veratridine modification of the purified sodium channel alpha-polypeptide from eel electroplax." Journal of General Physiology 94, no. 5 (1989): 813–31. http://dx.doi.org/10.1085/jgp.94.5.813.

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In the interest of continuing structure-function studies, highly purified sodium channel preparations from the eel electroplax were incorporated into planar lipid bilayers in the presence of veratridine. This lipoglycoprotein originates from muscle-derived tissue and consists of a single polypeptide. In this study it is shown to have properties analogous to sodium channels from another muscle tissue (Garber, S. S., and C. Miller. 1987. Journal of General Physiology. 89:459-480), which have an additional protein subunit. However, significant qualitative and quantitative differences were noted.

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4

Scheuer, T., and W. A. Catterall. "Control of neuronal excitability by phosphorylation and dephosphorylation of sodium channels." Biochemical Society Transactions 34, no. 6 (2006): 1299–302. http://dx.doi.org/10.1042/bst0341299.

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Currents through voltage-gated sodium channels drive action potential depolarization in neurons and other excitable cells. Smaller currents through these channels are key components of currents that control neuronal firing and signal integration. Changes in sodium current have profound effects on neuronal firing. Sodium channels are controlled by neuromodulators acting through phosphorylation of the channel by serine/threonine and tyrosine protein kinases. That phosphorylation requires specific molecular interaction of kinases and phosphatases with the channel molecule to form localized signal

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5

Barnes, S., and B. Hille. "Veratridine modifies open sodium channels." Journal of General Physiology 91, no. 3 (1988): 421–43. http://dx.doi.org/10.1085/jgp.91.3.421.

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The state dependence of Na channel modification by the alkaloid neurotoxin veratridine was investigated with single-channel and whole-cell voltage-clamp recording in neuroblastoma cells. Several tests of whole-cell Na current behavior in the presence of veratridine supported the hypothesis that Na channels must be open in order to undergo modification by the neurotoxin. Modification was use dependent and required depolarizing pulses, the voltage dependence of production of modified channels was similar to that of normal current activation, and prepulses that caused inactivation of normal curre

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6

Huguenard, John R. "Sodium Channels." Neuron 33, no. 4 (2002): 492–94. http://dx.doi.org/10.1016/s0896-6273(02)00592-5.

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7

Wood, John N., and Federico Iseppon. "Sodium channels." Brain and Neuroscience Advances 2 (January 2018): 239821281881068. http://dx.doi.org/10.1177/2398212818810684.

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In 2000, with the completion of the human genome project, nine related channels were found to comprise the complete voltage-gated sodium gene family and they were renamed NaV1.1–NaV1.9. This millennial event reflected the extraordinary impact of molecular genetics on our understanding of electrical signalling in the nervous system. In this review, studies of animal electricity from the time of Galvani to the present day are described. The seminal experiments and models of Hodgkin and Huxley coupled with the discovery of the structure of DNA, the genetic code and the application of molecular ge

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8

Yatani, A., D. L. Kunze, and A. M. Brown. "Effects of dihydropyridine calcium channel modulators on cardiac sodium channels." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 1 (1988): H140—H147. http://dx.doi.org/10.1152/ajpheart.1988.254.1.h140.

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To investigate whether cardiac sodium channels have dihydropyridine (DHP) receptors we studied the effects of the optically pure (greater than 95%) enantiomers of the DHPs PN200–110 and BAY-K 8644 and the racemic DHP nitrendipine (NTD). Whole cell and single-channel sodium currents were recorded from cultured ventricular cells of neonatal rats using the patch-clamp method. NTD reduced cardiac sodium currents in a voltage-dependent manner. Inhibitory effects were due to an increase in traces without activity. The unit conductance remained unchanged. At negative holding potentials, NTD transient

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9

Segal, Michael M., and Andrea F. Douglas. "Late Sodium Channel Openings Underlying Epileptiform Activity Are Preferentially Diminished by the Anticonvulsant Phenytoin." Journal of Neurophysiology 77, no. 6 (1997): 3021–34. http://dx.doi.org/10.1152/jn.1997.77.6.3021.

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Segal, Michael M. and Andrea F. Douglas. Late sodium channel openings underlying epileptiform activity are preferentially diminished by the anticonvulsant phenytoin. J. Neurophysiol. 77: 3021–3034, 1997. Late openings of sodium channels were observed in outside-out patch recordings from hippocampal neurons in culture. In previous studies of such neurons, a persistent sodium current appeared to underlie the ictal epileptiform activity. All the channel currents were blocked by tetrodotoxin. In addition to the transient openings of sodium channels making up the peak sodium current, there were two

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10

Terlau, H., M. Stocker, K. J. Shon, J. M. McIntosh, and B. M. Olivera. "MicroO-conotoxin MrVIA inhibits mammalian sodium channels, but not through site I." Journal of Neurophysiology 76, no. 3 (1996): 1423–29. http://dx.doi.org/10.1152/jn.1996.76.3.1423.

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1. A 31-amino-acid peptide from the venom of the snail-hunting species Conus marmoreus, microO-conotoxin MrVIA, inhibits mammalian voltage-gated sodium channels through a novel mechanism distinct from saxitoxin, tetrodotoxin, or mu-conotoxin. 2. MicroO-Conotoxin MrVIA blocks rat brain type II sodium channels expressed in Xenopus oocytes (IC50 approximately 200 nM, Hill coefficient approximately 1.6 +/- 0.2, mean +/- SE). Channel activation/inactivation kinetics and current-voltage relationships were unperturbed. 3. MicroO-Conotoxin MrVIA does not cause phasic or use-dependent inhibition of sod

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11

Rehberg, Benno, and Daniel S. Duch. "Suppression of Central Nervous System Sodium Channels by Propofol." Anesthesiology 91, no. 2 (1999): 512–20. http://dx.doi.org/10.1097/00000542-199908000-00026.

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Background Previous studies have provided evidence that clinical levels of propofol alter the functions of voltage-dependent sodium channels, thereby inhibiting synaptic release of glutamate. However, most of these experiments were conducted in the presence of sodium-channel activators, which alter channel inactivation. This study electrophysiologically characterized the interactions of propofol with unmodified sodium channels. Methods Sodium currents were measured using whole-cell patch-clamp recordings of rat brain IIa sodium channels expressed in a stably transfected Chinese hamster ovary c

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12

Paillart, C., J. L. Boudier, J. A. Boudier, H. Rochat, F. Couraud, and B. Dargent. "Activity-induced internalization and rapid degradation of sodium channels in cultured fetal neurons." Journal of Cell Biology 134, no. 2 (1996): 499–509. http://dx.doi.org/10.1083/jcb.134.2.499.

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A regulatory mechanism for neuronal excitability consists in controlling sodium channel density at the plasma membrane. In cultured fetal neurons, activation of sodium channels by neurotoxins, e.g., veratridine and alpha-scorpion toxin (alpha-ScTx) that enhance the channel open state probability induced a rapid down-regulation of surface channels. Evidence that the initial step of activity-induced sodium channel down-regulation is mediated by internalization was provided by using 125I-alpha-ScTx as both a channel probe and activator. After its binding to surface channels, the distribution of 1

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13

Waxman, Stephen G. "The neuron as a dynamic electrogenic machine: modulation of sodium–channel expression as a basis for functional plasticity in neurons." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1394 (2000): 199–213. http://dx.doi.org/10.1098/rstb.2000.0559.

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Neurons signal each other via regenerative electrical impulses (action potentials) and thus can be thought of as electrogenic machines. V oltage–gated sodium channels produce the depolarizations necessary for action potential activity in most neurons and, in this respect, lie close to the heart of the electrogenic machinery. Although classical neurophysiological doctrine accorded ‘the’ sodium channel a crucial role in electrogenesis, it is now clear that nearly a dozen genes encode distinct sodium channels with different molecular structures and functional properties, and the majority of these

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14

Tomaselli, G. F., A. M. Feldman, G. Yellen, and E. Marban. "Human cardiac sodium channels expressed in Xenopus oocytes." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (1990): H903—H906. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h903.

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We report the expression of voltage-dependent Na+ channels in Xenopus oocytes injected with total RNA isolated from explanted human hearts. The expressed channels demonstrate characteristic voltage-dependent gating, inhibition by tetrodotoxin, and selectivity for Na+. Oocytes injected with sterile water or intentionally degraded RNA had no similar channel activity. The antiarrhythmic agent lidocaine (20 microM) inhibits current flow through the channel in a voltage-dependent fashion. Na+ channels expressed by injection of human cardiac RNA into Xenopus oocytes qualitatively resemble channels i

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15

Hahin, R. "Removal of inactivation causes time-invariant sodium current decays." Journal of General Physiology 92, no. 3 (1988): 331–50. http://dx.doi.org/10.1085/jgp.92.3.331.

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The kinetic properties of the closing of Na channels were studied in frog skeletal muscle to obtain information about the dependence of channel closing on the past history of the channel. Channel closing was studied in normal and modified channels. Chloramine-T was used to modify the channels so that inactivation was virtually removed. A series of depolarizing prepulse potentials was used to activate Na channels, and a -140-mV postpulse was used to monitor the closing of the channels. Unmodified channels decay via a biexponential process with time constants of 72 and 534 microseconds at 12 deg

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16

Takahashi, Izumi, and Masami Yoshino. "Functional coupling between sodium-activated potassium channels and voltage-dependent persistent sodium currents in cricket Kenyon cells." Journal of Neurophysiology 114, no. 4 (2015): 2450–59. http://dx.doi.org/10.1152/jn.00087.2015.

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In this study, we examined the functional coupling between Na+-activated potassium (KNa) channels and Na+ influx through voltage-dependent Na+ channels in Kenyon cells isolated from the mushroom body of the cricket Gryllus bimaculatus. Single-channel activity of KNa channels was recorded with the cell-attached patch configuration. The open probability ( Po) of KNa channels increased with increasing Na+ concentration in a bath solution, whereas it decreased by the substitution of Na+ with an equimolar concentration of Li+. The Po of KNa channels was also found to be reduced by bath application

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17

Rehberg, Benno, Yong-Hong Xiao, and Daniel S. Duch. "Central Nervous System Sodium Channels Are Significantly Suppressed at Clinical Concentrations of Volatile Anesthetics." Anesthesiology 84, no. 5 (1996): 1223–33. http://dx.doi.org/10.1097/00000542-199605000-00025.

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Background Although voltage-dependent sodium channels have been proposed as possible molecular sites of anesthetic action, they generally are considered too insensitive to be likely molecular targets. However, most previous molecular studies have used peripheral sodium channels as models. To examine the interactions of volatile anesthetics with mammalian central nervous system voltage-gated sodium channels, rat brain IIA sodium channels were expressed in a stably transfected Chinese hamster ovary cell line, and their modification by volatile anesthetics was examined. Methods Sodium currents we

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18

Lee, Sora, Samuel J. Goodchild, and Christopher A. Ahern. "Local anesthetic inhibition of a bacterial sodium channel." Journal of General Physiology 139, no. 6 (2012): 507–16. http://dx.doi.org/10.1085/jgp.201210779.

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Recent structural breakthroughs with the voltage-gated sodium channel from Arcobacter butzleri suggest that such bacterial channels may provide a structural platform to advance the understanding of eukaryotic sodium channel gating and pharmacology. We therefore set out to determine whether compounds known to interact with eukaryotic NaVs could also inhibit the bacterial channel from Bacillus halodurans and NaChBac and whether they did so through similar mechanisms as in their eukaryotic homologues. The data show that the archetypal local anesthetic (LA) lidocaine inhibits resting NaChBac chann

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19

Davis, Scott F., and Cindy L. Linn. "Mechanism linking NMDA receptor activation to modulation of voltage-gated sodium current in distal retina." American Journal of Physiology-Cell Physiology 284, no. 5 (2003): C1193—C1204. http://dx.doi.org/10.1152/ajpcell.00256.2002.

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In this study, we investigated the mechanism that links activation of N-methyl-D-aspartate (NMDA) receptors to inhibition of voltage-gated sodium channels in isolated catfish cone horizontal cells. NMDA channels were activated in voltage-clamped cells incubated in low-calcium saline or dialyzed with the calcium chelator BAPTA to determine that calcium influx through NMDA channels is required for sodium channel modulation. To determine whether calcium influx through NMDA channels triggers calcium-induced calcium release (CICR), cells were loaded with the calcium-sensitive dye calcium green 2 an

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20

Althaus, Mike, Wolfgang G. Clauss, and Martin Fronius. "Amiloride-Sensitive Sodium Channels and Pulmonary Edema." Pulmonary Medicine 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/830320.

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The development of pulmonary edema can be considered as a combination of alveolar flooding via increased fluid filtration, impaired alveolar-capillary barrier integrity, and disturbed resolution due to decreased alveolar fluid clearance. An important mechanism regulating alveolar fluid clearance is sodium transport across the alveolar epithelium. Transepithelial sodium transport is largely dependent on the activity of sodium channels in alveolar epithelial cells. This paper describes how sodium channels contribute to alveolar fluid clearance under physiological conditions and how deregulation

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21

Garty, H., and L. G. Palmer. "Epithelial sodium channels: function, structure, and regulation." Physiological Reviews 77, no. 2 (1997): 359–96. http://dx.doi.org/10.1152/physrev.1997.77.2.359.

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The apical (outward-facing) membranes of high-resistance epithelia contain Na+ channels, traditionally identified by their sensitivity to block by the K(+)-sparing diuretic amiloride. Such channels have been characterized in amphibian skin and urinary bladder, renal collecting duct, distal colon, sweat and salivary glands, lung, and taste buds. They mediate the first step of active Na+ reabsorption and play a major role in the maintenance of electrolyte and water homeostasis in all vertebrates. In the past, these channels were classified according to their biophysical and pharmacological prope

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22

Ban, Yue, Benjamin E. Smith, and Michael R. Markham. "A highly polarized excitable cell separates sodium channels from sodium-activated potassium channels by more than a millimeter." Journal of Neurophysiology 114, no. 1 (2015): 520–30. http://dx.doi.org/10.1152/jn.00475.2014.

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The bioelectrical properties and resulting metabolic demands of electrogenic cells are determined by their morphology and the subcellular localization of ion channels. The electric organ cells (electrocytes) of the electric fish Eigenmannia virescens generate action potentials (APs) with Na+ currents >10 μA and repolarize the AP with Na+-activated K+ (KNa) channels. To better understand the role of morphology and ion channel localization in determining the metabolic cost of electrocyte APs, we used two-photon three-dimensional imaging to determine the fine cellular morphology and immunohist

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23

Tousson, A., C. D. Alley, E. J. Sorscher, B. R. Brinkley, and D. J. Benos. "Immunochemical localization of amiloride-sensitive sodium channels in sodium-transporting epithelia." Journal of Cell Science 93, no. 2 (1989): 349–62. http://dx.doi.org/10.1242/jcs.93.2.349.

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The localization of amiloride-sensitive Na+ channels in Na+-transporting epithelia was examined using antibodies made against amiloride-binding Na+ channel protein purified from bovine kidney. The distribution of the channel protein was determined in thick frozen sections at the light-microscopic level using indirect immunofluorescence, and at the electron-microscopic level using immunogold labelling. In the cells of both the intact bovine collecting tubule and A6 confluent monolayers, only the luminal or apical-facing surface membranes showed staining. Sodium channel protein was characteristi

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Stocker, Patrick J., and Eric S. Bennett. "Differential Sialylation Modulates Voltage-gated Na+ Channel Gating throughout the Developing Myocardium." Journal of General Physiology 127, no. 3 (2006): 253–65. http://dx.doi.org/10.1085/jgp.200509423.

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Voltage-gated sodium channel function from neonatal and adult rat cardiomyocytes was measured and compared. Channels from neonatal ventricles required an ∼10 mV greater depolarization for voltage-dependent gating events than did channels from neonatal atria and adult atria and ventricles. We questioned whether such gating shifts were due to developmental and/or chamber-dependent changes in channel-associated functional sialic acids. Thus, all gating characteristics for channels from neonatal atria and adult atria and ventricles shifted significantly to more depolarized potentials after removal

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Worley, J. F., R. J. French, and B. K. Krueger. "Trimethyloxonium modification of single batrachotoxin-activated sodium channels in planar bilayers. Changes in unit conductance and in block by saxitoxin and calcium." Journal of General Physiology 87, no. 2 (1986): 327–49. http://dx.doi.org/10.1085/jgp.87.2.327.

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Single batrachotoxin-activated sodium channels from rat brain were modified by trimethyloxonium (TMO) after incorporation in planar lipid bilayers. TMO modification eliminated saxitoxin (STX) sensitivity, reduced the single channel conductance by 37%, and reduced calcium block of inward sodium currents. These effects always occurred concomitantly, in an all-or-none fashion. Calcium and STX protected sodium channels from TMO modification with potencies similar to their affinities for block. Calcium inhibited STX binding to rat brain membrane vesicles and relieved toxin block of channels in bila

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Payandeh, Jian. "Crystallographic studies of voltage-gated sodium and calcium channels." Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C1488. http://dx.doi.org/10.1107/s2053273314085118.

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Voltage-gated ion channels (VGICs) mediate electrical signaling within the nervous system and regulate a wide range of physiological processes. Voltage-gated sodium (Nav) channels are responsible for initiating action potentials and their rapid activation, sodium selectivity, and drug sensitivity are unique among VGICs. Nav channels are the molecular targets of drugs used in local anaesthesia and in the treatment of genetic and sporadic Nav channelopathies including inherited epilepsy, migraine, periodic paralysis, cardiac arrhythmia, and chronic pain syndromes. Recent crystal structures of a

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27

Stern, M., R. Kreber, and B. Ganetzky. "Dosage effects of a Drosophila sodium channel gene on behavior and axonal excitability." Genetics 124, no. 1 (1990): 133–43. http://dx.doi.org/10.1093/genetics/124.1.133.

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Abstract The effects of para mutations on behavior and axonal excitability in Drosophila suggested that para specifically affects sodium channels. This hypothesis was confirmed by molecular analysis of the para locus, which demonstrates that the encoded para product is a sodium channel polypeptide. Here we characterize the effects of altered para+ dosage on behavior and axonal excitability, both in an otherwise wild-type background and in combination with two other mutations: napts, which also affects sodium channels, and ShKS133, which specifically affects potassium channels. Whereas it was p

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Qiu, W., B. Lee, M. Lancaster, W. Xu, S. Leung, and S. E. Guggino. "Cyclic nucleotide-gated cation channels mediate sodium and calcium influx in rat colon." American Journal of Physiology-Cell Physiology 278, no. 2 (2000): C336—C343. http://dx.doi.org/10.1152/ajpcell.2000.278.2.c336.

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We found mRNA for the three isoforms of the cyclic nucleotide-gated nonselective cation channel expressed in the mucosal layer of the rat intestine from the duodenum to the colon and in intestinal epithelial cell lines in culture. Because these channels are permeable to sodium and calcium and are stimulated by cGMP or cAMP, we measured 8-bromo-cGMP-stimulated sodium-mediated short-circuit current ( I sc) in proximal and distal colon and unidirectional45Ca2+fluxes in proximal colon to determine whether these channels could mediate transepithelial sodium and calcium absorption across the colon.

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McEwen, Dyke P., та Lori L. Isom. "Heterophilic Interactions of Sodium Channel β1 Subunits with Axonal and Glial Cell Adhesion Molecules". Journal of Biological Chemistry 279, № 50 (2004): 52744–52. http://dx.doi.org/10.1074/jbc.m405990200.

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Voltage-gated sodium channels localize at high density in axon initial segments and nodes of Ranvier in myelinated axons. Sodium channels consist of a pore-forming α subunit and at least one β subunit. β1 is a member of the immunoglobulin superfamily of cell adhesion molecules and interacts homophilically and heterophilically with contactin and Nf186. In this study, we characterized β1 interactions with contactin and Nf186 in greater detail and investigated interactions of β1 with NrCAM, Nf155, and sodium channel β2 and β3 subunits. Using Fc fusion proteins and immunocytochemical techniques, w

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Vais, Horia, Martin S. Williamson, Susannah J. Goodson, et al. "Activation of Drosophila Sodium Channels Promotes Modification by Deltamethrin." Journal of General Physiology 115, no. 3 (2000): 305–18. http://dx.doi.org/10.1085/jgp.115.3.305.

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kdr and super-kdr are mutations in houseflies and other insects that confer 30- and 500-fold resistance to the pyrethroid deltamethrin. They correspond to single (L1014F) and double (L1014F+M918T) mutations in segment IIS6 and linker II(S4–S5) of Na channels. We expressed Drosophila para Na channels with and without these mutations and characterized their modification by deltamethrin. All wild-type channels can be modified by &lt;10 nM deltamethrin, but high affinity binding requires channel opening: (a) modification is promoted more by trains of brief depolarizations than by a single long

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Vinson, Valda. "Targeting sodium channels." Science 363, no. 6433 (2019): 1296.7–1297. http://dx.doi.org/10.1126/science.363.6433.1296-g.

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Rossier, Bernard C., Cecilia M. Canessa, Laurent Schild, and Jean-Daniel Horisberger. "Epithelial sodium channels." Current Opinion in Nephrology and Hypertension 3, no. 5 (1994): 487–96. http://dx.doi.org/10.1097/00041552-199409000-00003.

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Keller, B. U., R. P. Hartshorne, J. A. Talvenheimo, W. A. Catterall, and M. Montal. "Sodium channels in planar lipid bilayers. Channel gating kinetics of purified sodium channels modified by batrachotoxin." Journal of General Physiology 88, no. 1 (1986): 1–23. http://dx.doi.org/10.1085/jgp.88.1.1.

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Single channel currents of sodium channels purified from rat brain and reconstituted into planar lipid bilayers were recorded. The kinetics of channel gating were investigated in the presence of batrachotoxin to eliminate inactivation and an analysis was conducted on membranes with a single active channel at any given time. Channel opening is favored by depolarization and is strongly voltage dependent. Probability density analysis of dwell times in the closed and open states of the channel indicates the occurrence of one open state and several distinct closed states in the voltage (V) range-12

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Stadnicka, Anna, Wai-Meng Kwok, Hali A. Hartmann, and Zeljko J. Bosnjak. "Effects of Halothane and Isoflurane on Fast and Slow Inactivation of Human Heart hH1a Sodium Channels." Anesthesiology 90, no. 6 (1999): 1671–83. http://dx.doi.org/10.1097/00000542-199906000-00024.

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Background Cloning and heterologous expression of ion channels allow biophysical and molecular studies of the mechanisms of volatile anesthetic interactions with human heart sodium channels. Volatile anesthetics may influence the development of arrhythmias arising from cardiac sodium channel dysfunction. For that reason, understanding the mechanisms of interactions between these anesthetics and cardiac sodium channels is important. This study evaluated the mechanisms of volatile anesthetic actions on the cloned human cardiac sodium channel (hH1a) alpha subunit. Methods Inward sodium currents w

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Wu, Xin, and Liang Hong. "Calmodulin Interactions with Voltage-Gated Sodium Channels." International Journal of Molecular Sciences 22, no. 18 (2021): 9798. http://dx.doi.org/10.3390/ijms22189798.

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Calmodulin (CaM) is a small protein that acts as a ubiquitous signal transducer and regulates neuronal plasticity, muscle contraction, and immune response. It interacts with ion channels and plays regulatory roles in cellular electrophysiology. CaM modulates the voltage-gated sodium channel gating process, alters sodium current density, and regulates sodium channel protein trafficking and expression. Many mutations in the CaM-binding IQ domain give rise to diseases including epilepsy, autism, and arrhythmias by interfering with CaM interaction with the channel. In the present review, we discus

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Duszyk, Marek, Andrew S. French, and S. F. Paul Man. "Cystic fibrosis affects chloride and sodium channels in human airway epithelia." Canadian Journal of Physiology and Pharmacology 67, no. 10 (1989): 1362–65. http://dx.doi.org/10.1139/y89-217.

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Abnormalities of epithelial function in cystic fibrosis (CF) have been linked to defects in cell membrane permeability to chloride or sodium ions. Recently, a class of chloride channels in airway epithelial cells have been reported to lack their usual sensitivity to phosphorylation via cAMP-dependent protein kinase, suggesting that CF could be due to a single genetic defect in these channels. We have examined single chloride and sodium channels in control and CF human nasal epithelia using the patch-clamp technique. The most common chloride channel was not the one previously associated with CF

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Liin, Sara I., Per-Eric Lund, Johan E. Larsson, Johan Brask, Björn Wallner, and Fredrik Elinder. "Biaryl sulfonamide motifs up- or down-regulate ion channel activity by activating voltage sensors." Journal of General Physiology 150, no. 8 (2018): 1215–30. http://dx.doi.org/10.1085/jgp.201711942.

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Voltage-gated ion channels are key molecules for the generation of cellular electrical excitability. Many pharmaceutical drugs target these channels by blocking their ion-conducting pore, but in many cases, channel-opening compounds would be more beneficial. Here, to search for new channel-opening compounds, we screen 18,000 compounds with high-throughput patch-clamp technology and find several potassium-channel openers that share a distinct biaryl-sulfonamide motif. Our data suggest that the negatively charged variants of these compounds bind to the top of the voltage-sensor domain, between t

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Ratnakumari, Lingamaneni, and Hugh C. Hemmings. "Inhibition of Presynaptic Sodium Channels by Halothane." Anesthesiology 88, no. 4 (1998): 1043–54. http://dx.doi.org/10.1097/00000542-199804000-00025.

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Background Recent electrophysiologic studies indicate that clinical concentrations of volatile general anesthetic agents inhibit central nervous system sodium (Na+) channels. In this study, the biochemical effects of halothane on Na+ channel function were determined using rat brain synaptosomes (pinched-off nerve terminals) to assess the role of presynaptic Na+ channels in anesthetic effects. Methods Synaptosomes from adult rat cerebral cortex were used to determine the effects of halothane on veratridine-evoked Na+ channel-dependent Na+ influx (using 22Na+), changes in intrasynaptosomal [Na+]

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Campos, Fabiana V., Baron Chanda, Paulo S. L. Beirão та Francisco Bezanilla. "β-Scorpion Toxin Modifies Gating Transitions in All Four Voltage Sensors of the Sodium Channel". Journal of General Physiology 130, № 3 (2007): 257–68. http://dx.doi.org/10.1085/jgp.200609719.

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Several naturally occurring polypeptide neurotoxins target specific sites on the voltage-gated sodium channels. Of these, the gating modifier toxins alter the behavior of the sodium channels by stabilizing transient intermediate states in the channel gating pathway. Here we have used an integrated approach that combines electrophysiological and spectroscopic measurements to determine the structural rearrangements modified by the β-scorpion toxin Ts1. Our data indicate that toxin binding to the channel is restricted to a single binding site on domain II voltage sensor. Analysis of Cole-Moore sh

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Vanoye, Carlos G., Christoph Lossin, Thomas H. Rhodes, and Alfred L. George. "Single-channel Properties of Human NaV1.1 and Mechanism of Channel Dysfunction in SCN1A-associated Epilepsy." Journal of General Physiology 127, no. 1 (2005): 1–14. http://dx.doi.org/10.1085/jgp.200509373.

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Mutations in genes encoding neuronal voltage-gated sodium channel subunits have been linked to inherited forms of epilepsy. The majority of mutations (&gt;100) associated with generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI) occur in SCN1A encoding the NaV1.1 neuronal sodium channel α-subunit. Previous studies demonstrated functional heterogeneity among mutant SCN1A channels, revealing a complex relationship between clinical and biophysical phenotypes. To further understand the mechanisms responsible for mutant SCN1A behavior, we perfo

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Gray, Richard, and Daniel Johnston. "Sodium sensitivity of KNa channels in mouse CA1 neurons." Journal of Neurophysiology 125, no. 5 (2021): 1690–97. http://dx.doi.org/10.1152/jn.00064.2021.

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We studied KNa channels in mouse hippocampal CA1 neurons. Excised inside-out patches showed the channels to be prevalent and active in most patches in the presence of Na+. Cell-attached recordings from intact neurons, however, showed little channel activity. Increasing cytoplasmic sodium in intact cells showed a small effect on channel activity compared with that seen in inside-out excised patches. Blockade of the Na+/K+ pump with ouabain, however, restored the activity of the channels to that seen in inside-out patches.

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Perez-Pinzon, M. A., M. Rosenthal, T. J. Sick, P. L. Lutz, J. Pablo, and D. Mash. "Downregulation of sodium channels during anoxia: a putative survival strategy of turtle brain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 4 (1992): R712—R715. http://dx.doi.org/10.1152/ajpregu.1992.262.4.r712.

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In contrast to mammalian brain, which exhibits rapid degeneration during anoxia, the brains of certain species of turtles show an extraordinary capacity to survive prolonged anoxia. The decrease in energy expenditure shown by the anoxic turtle brain is likely to be a key factor for anoxic survival. The "channel arrest" hypothesis proposes that ion channels, which regulate brain electrical activity in normoxia, may be altered during anoxia in the turtle brain as a mechanism to spare energy. Goals of present research were to test this hypothesis and to determine whether down-regulation of sodium

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JEZIORSKI, M. C., R. M. GREENBERG, and P. A. V. ANDERSON. "Cloning of a putative voltage-gated sodium channel from the turbellarian flatworm Bdelloura candida." Parasitology 115, no. 3 (1997): 289–96. http://dx.doi.org/10.1017/s0031182097001388.

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The neuromuscular sodium currents of early invertebrates such as platyhelminths display distinctive kinetic and pharmacological properties. We have cloned a cDNA from the horseshoe crab flatworm Bdelloura candida that encodes a protein homologous to the primary subunit of voltage-gated sodium channels. The B. candida protein, named BdNa1, exhibits amino acid identity of 40–47% to sodium channels of vertebrates and higher invertebrates. BdNa1 has the multidomain structure characteristic of sodium channels, and is most highly conserved in the hydrophobic transmembrane segments and the regions th

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Negulyaev, Y. A., E. A. Vedernikova, and A. V. Maximov. "Disruption of actin filaments increases the activity of sodium-conducting channels in human myeloid leukemia cells." Molecular Biology of the Cell 7, no. 12 (1996): 1857–64. http://dx.doi.org/10.1091/mbc.7.12.1857.

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With the use of the patch clamp technique, the role of cytoskeleton in the regulation of ion channels in plasma membrane of leukemic K562 cells was examined. Single-channel measurements have indicated that disruption of actin filaments with cytochalasin D (CD) resulted in a considerable increase of the activity of non-voltage-gated sodium-permeable channels of 12 pS unitary conductance. Background activity of these channels was low; open probability (po) did not exceed 0.01-0.02. After CD, po grew at least 10-20 times. Cell-attached and whole-cell recordings showed that activation of sodium ch

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Ratnakumari, L., and H. C. Hemmings. "Effects of Propofol on Sodium Channel-dependent Sodium Influx and Glutamate Release in Rat Cerebrocortical Synaptosomes." Anesthesiology 86, no. 2 (1997): 428–39. http://dx.doi.org/10.1097/00000542-199702000-00018.

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Background Previous electrophysiologic studies have implicated voltage-dependent Na+ channels as a molecular site of action for propofol. This study considered the effects of propofol on Na+ channel-mediated Na+ influx and neurotransmitter release in rat brain synaptosomes (isolated presynaptic nerve terminals). Methods Purified cerebrocortical synaptosomes from adult rats were used to determine the effects of propofol on Na+ influx through voltage-dependent Na+ channels (measured using 22Na+) and intracellular [Na+] (measured by ion-specific spectrofluorimetry). For comparison, the effects of

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Behrens, M. I., A. Oberhauser, F. Bezanilla, and R. Latorre. "Batrachotoxin-modified sodium channels from squid optic nerve in planar bilayers. Ion conduction and gating properties." Journal of General Physiology 93, no. 1 (1989): 23–41. http://dx.doi.org/10.1085/jgp.93.1.23.

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Squid optic nerve sodium channels were characterized in planar bilayers in the presence of batrachotoxin (BTX). The channel exhibits a conductance of 20 pS in symmetrical 200 mM NaCl and behaves as a sodium electrode. The single-channel conductance saturates with increasing the concentration of sodium and the channel conductance vs. sodium concentration relation is well described by a simple rectangular hyperbola. The apparent dissociation constant of the channel for sodium is 11 mM and the maximal conductance is 23 pS. The selectivity determined from reversal potentials obtained in mixed ioni

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Docken, Steffen S., Colleen E. Clancy, and Timothy J. Lewis. "Rate-dependent effects of lidocaine on cardiac dynamics: Development and analysis of a low-dimensional drug-channel interaction model." PLOS Computational Biology 17, no. 6 (2021): e1009145. http://dx.doi.org/10.1371/journal.pcbi.1009145.

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State-dependent sodium channel blockers are often prescribed to treat cardiac arrhythmias, but many sodium channel blockers are known to have pro-arrhythmic side effects. While the anti and proarrhythmic potential of a sodium channel blocker is thought to depend on the characteristics of its rate-dependent block, the mechanisms linking these two attributes are unclear. Furthermore, how specific properties of rate-dependent block arise from the binding kinetics of a particular drug is poorly understood. Here, we examine the rate-dependent effects of the sodium channel blocker lidocaine by const

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Ohara, A., H. Matsunaga, and D. C. Eaton. "G protein activation inhibits amiloride-blockable highly selective sodium channels in A6 cells." American Journal of Physiology-Cell Physiology 264, no. 2 (1993): C352—C360. http://dx.doi.org/10.1152/ajpcell.1993.264.2.c352.

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Single-channel methods were used to examine the regulation of amiloride-blockable highly selective sodium channels by guanine nucleotide-binding proteins (G proteins). A6 cells (a renal cell line derived from Xenopus laevis kidney) were cultured on permeable collagen films, and patch recordings were made from the apical membranes of confluent cells. The predominant channel in the apical membranes is a highly selective, 4-pS, amiloride-blockable sodium channel (the Na(+)-to-K+ permeability ratio is > 30). In inside-out patches, application to the cytosolic surface of guanosine-5'-O-(2-thiodi

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Ghovanloo, Mohammad-Reza, Noah Gregory Shuart, Janette Mezeyova, Richard A. Dean, Peter C. Ruben, and Samuel J. Goodchild. "Inhibitory effects of cannabidiol on voltage-dependent sodium currents." Journal of Biological Chemistry 293, no. 43 (2018): 16546–58. http://dx.doi.org/10.1074/jbc.ra118.004929.

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Cannabis sativa contains many related compounds known as phytocannabinoids. The main psychoactive and nonpsychoactive compounds are Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD), respectively. Much of the evidence for clinical efficacy of CBD-mediated antiepileptic effects has been from case reports or smaller surveys. The mechanisms for CBD's anticonvulsant effects are unclear and likely involve noncannabinoid receptor pathways. CBD is reported to modulate several ion channels, including sodium channels (Nav). Evaluating the therapeutic mechanisms and safety of CBD demands a richer unde

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Ahern, Christopher A., Jian Payandeh, Frank Bosmans, and Baron Chanda. "The hitchhiker’s guide to the voltage-gated sodium channel galaxy." Journal of General Physiology 147, no. 1 (2015): 1–24. http://dx.doi.org/10.1085/jgp.201511492.

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Eukaryotic voltage-gated sodium (Nav) channels contribute to the rising phase of action potentials and served as an early muse for biophysicists laying the foundation for our current understanding of electrical signaling. Given their central role in electrical excitability, it is not surprising that (a) inherited mutations in genes encoding for Nav channels and their accessory subunits have been linked to excitability disorders in brain, muscle, and heart; and (b) Nav channels are targeted by various drugs and naturally occurring toxins. Although the overall architecture and behavior of these

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