The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
Yoshiji Okazaki - One of the best experts on this subject based on the ideXlab platform.
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temporal relationship between cytosolic free ca2 and Membrane potential during hypotonic turgor regulation in a brackish water charophyte lamprothamnium succinctum
Plant and Cell Physiology, 2002Co-Authors: Yoshiji Okazaki, Mitsuo Ishigami, N IwasakiAbstract:Internodal cells of a brackish water charophyte, Lamprothamnium succinctum, regulate turgor pressure in response to changes in external osmotic pressure by modifying vacuolar concentrations of KCl. An increase in cytosolic concentration of free Ca 2 + ([Ca 2 + ] c ) is necessary for the progress of turgor regulation induced by hypotonic treatment. Initial changes in Membrane potential and [Ca 2 + ] c upon hypotonic treatment were measured to examine the temporal relationship between the two parameters. Fura-dextran (potassium salt, M r 10,000, anionic) that had been injected into the cytosol was used to measure [Ca 2 + ] c . Membrane potential and Membrane Conductance under a current-clamp condition were also measured. Decrease in external osmotic pressure by 0.16 Osm induced a simultaneous increase in [Ca 2 + ] c with both depolarization of the Membrane and increase in the Membrane Conductance. Decrease in external osmotic pressure by 0.05 Osm induced a simultaneous increase in [Ca 2 + ] c with Membrane depolarization but the increase in Membrane Conductance started later than the other two processes. There was a close temporal relationship between the increase in [Ca 2 + ] c and Membrane depolarization on the initial response of turgor regulation induced by hypotonic treatment.
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Turgor regulation in a brackish water charophyte,Lamprothamnium succinctum
Journal of Plant Research, 1996Co-Authors: Yoshiji OkazakiAbstract:Internodal cells of a brackish water charophyte, Lamprothamnium succinctum (A. Br. in Ash.) R.D.W. regulate the turgor pressure in response to changes in both the cellular and the external osmotic pressures. During turgor regulation upon hypotonic treatment, net effluxes of K^+ and Cl^− from the vacuole, Membrane depolarization, a transient increase in the electrical Membrane Conductance and a transient increase in concentration of cytoplasmic Ca^2+ are induced. Activation of the plasmalemma Ca^2+ channels and the Ca^2+-controlled passive effluxes of K^+ and Cl^− through the plasmalemma ion channels are postulated.
N Iwasaki - One of the best experts on this subject based on the ideXlab platform.
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temporal relationship between cytosolic free ca2 and Membrane potential during hypotonic turgor regulation in a brackish water charophyte lamprothamnium succinctum
Plant and Cell Physiology, 2002Co-Authors: Yoshiji Okazaki, Mitsuo Ishigami, N IwasakiAbstract:Internodal cells of a brackish water charophyte, Lamprothamnium succinctum, regulate turgor pressure in response to changes in external osmotic pressure by modifying vacuolar concentrations of KCl. An increase in cytosolic concentration of free Ca 2 + ([Ca 2 + ] c ) is necessary for the progress of turgor regulation induced by hypotonic treatment. Initial changes in Membrane potential and [Ca 2 + ] c upon hypotonic treatment were measured to examine the temporal relationship between the two parameters. Fura-dextran (potassium salt, M r 10,000, anionic) that had been injected into the cytosol was used to measure [Ca 2 + ] c . Membrane potential and Membrane Conductance under a current-clamp condition were also measured. Decrease in external osmotic pressure by 0.16 Osm induced a simultaneous increase in [Ca 2 + ] c with both depolarization of the Membrane and increase in the Membrane Conductance. Decrease in external osmotic pressure by 0.05 Osm induced a simultaneous increase in [Ca 2 + ] c with Membrane depolarization but the increase in Membrane Conductance started later than the other two processes. There was a close temporal relationship between the increase in [Ca 2 + ] c and Membrane depolarization on the initial response of turgor regulation induced by hypotonic treatment.
Thomas Holm Pedersen - One of the best experts on this subject based on the ideXlab platform.
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depletion of atp limits Membrane excitability of skeletal muscle by increasing both clc1 open probability and Membrane Conductance
Frontiers in Neurology, 2020Co-Authors: Pieter Arnold Leermakers, Frank Vincenzo De Paoli, Kamilla Lohde Tordrup Dybdahl, Kristian Soborg Husted, Anders Riisager, Tomas Pinos, John Vissing, Thomas Krag, Thomas Holm PedersenAbstract:Activation of skeletal muscle contractions require that action potentials can be excited and propagated along the muscle fibers. Recent studies have revealed that muscle fiber excitability is regulated during repeated firing of action potentials by cellular signaling systems that control the function of ion channel that determine the resting Membrane Conductance (G (m) ). In fast-twitch muscle, prolonged firing of action potentials triggers a marked increase in G (m) , reducing muscle fiber excitability and causing action potential failure. Both ClC-1 and K(ATP) ion channels contribute to this G (m) rise, but the exact molecular regulation underlying their activation remains unclear. Studies in expression systems have revealed that ClC-1 is able to bind adenosine nucleotides, and that low adenosine nucleotide levels result in ClC-1 activation. In three series of experiments, this study aimed to explore whether ClC-1 is also regulated by adenosine nucleotides in native skeletal muscle fibers, and whether the adenosine nucleotide sensitivity of ClC-1 could explain the rise in G (m) muscle fibers during prolonged action potential firing. First, whole cell patch clamping of mouse muscle fibers demonstrated that ClC-1 activation shifted in the hyperpolarized direction when clamping pipette solution contained 0 mM ATP compared with 5 mM ATP. Second, three-electrode G (m) measurement during muscle fiber stimulation showed that glycolysis inhibition, with 2-deoxy-glucose or iodoacetate, resulted in an accelerated and rapid >400% G (m) rise during short periods of repeated action potential firing in both fast-twitch and slow-twitch rat, and in human muscle fibers. Moreover, ClC-1 inhibition with 9-anthracenecarboxylic acid resulted in either an absence or blunted G (m) rise during action potential firing in human muscle fibers. Third, G (m) measurement during repeated action potential firing in muscle fibers from a murine McArdle disease model suggest that the rise in G (m) was accelerated in a subset of fibers. Together, these results are compatible with ClC-1 function being regulated by the level of adenosine nucleotides in native tissue, and that the channel operates as a sensor of skeletal muscle metabolic state, limiting muscle excitability when energy status is low.
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comparison of regulated passive Membrane Conductance in action potential firing fast and slow twitch muscle
The Journal of General Physiology, 2009Co-Authors: Thomas Holm Pedersen, William Macdonald, Frank Vincenzo De Paoli, Iman S Gurung, Ole Baekgaard NielsenAbstract:In several pathological and experimental conditions, the passive Membrane Conductance of muscle fibers (Gm) and their excitability are inversely related. Despite this capacity of Gm to determine muscle excitability, its regulation in active muscle fibers is largely unexplored. In this issue, our previous study (Pedersen et al. 2009. J. Gen. Physiol. doi:10.1085/jgp.200910291) established a technique with which biphasic regulation of Gm in action potential (AP)-firing fast-twitch fibers of rat extensor digitorum longus muscles was identified and characterized with temporal resolution of seconds. This showed that AP firing initially reduced Gm via ClC-1 channel inhibition but after ∼1,800 APs, Gm rose substantially, causing AP excitation failure. This late increase of Gm reflected activation of ClC-1 and KATP channels. The present study has explored regulation of Gm in AP-firing slow-twitch fibers of soleus muscle and compared it to Gm dynamics in fast-twitch fibers. It further explored aspects of the cellular signaling that conveyed regulation of Gm in AP-firing fibers. Thus, in both fiber types, AP firing first triggered protein kinase C (PKC)-dependent ClC-1 channel inhibition that reduced Gm by ∼50%. Experiments with dantrolene showed that AP-triggered SR Ca2+ release activated this PKC-mediated ClC-1 channel inhibition that was associated with reduced rheobase current and improved function of depolarized muscles, indicating that the reduced Gm enhanced muscle fiber excitability. In fast-twitch fibers, the late rise in Gm was accelerated by glucose-free conditions, whereas it was postponed when intermittent resting periods were introduced during AP firing. Remarkably, elevation of Gm was never encountered in AP-firing slow-twitch fibers, even after 15,000 APs. These observations implicate metabolic depression in the elevation of Gm in AP-firing fast-twitch fibers. It is concluded that regulation of Gm is a general phenomenon in AP-firing muscle, and that differences in Gm regulation may contribute to the different phenotypes of fast- and slow-twitch muscle.
Mary J Beilby - One of the best experts on this subject based on the ideXlab platform.
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Salt tolerance at single cell level in giant-celled Characeae.
Frontiers in Plant Science, 2015Co-Authors: Mary J BeilbyAbstract:Characean plants provide an excellent experimental system for electrophysiology and physiology due to: (i) very large cell size, (ii) position on phylogenetic tree near the origin of land plants and (iii) continuous spectrum from very salt sensitive to very salt tolerant species. A range of experimental techniques is described, some unique to characean plants. Application of these methods provided electrical characteristics of Membrane transporters, which dominate the Membrane Conductance under different outside conditions. With this considerable background knowledge the electrophysiology of salt sensitive and salt tolerant genera can be compared under salt and/or osmotic stress. Both salt tolerant and salt sensitive Characeae show a rise in Membrane Conductance and simultaneous increase in Na+ influx upon exposure to saline medium. Salt tolerant Chara longifolia and Lamprothamnium sp. exhibit proton pump stimulation upon both turgor decrease and salinity increase, allowing the Membrane PD to remain negative. The turgor is regulated through the inward K+ rectifier and 2H+/Cl- symporter. Lamprothamnium plants can survive in hypersaline media up to twice seawater strength and withstand large sudden changes in salinity. Salt-sensitive Chara australis succumbs to 50 - 100 mM NaCl in few days. Cells exhibit no pump stimulation upon turgor decrease and at best transient pump stimulation upon salinity increase. Turgor is not regulated. The Membrane PD exhibits characteristic noise upon exposure to salinity. Depolarization of Membrane PD to excitation threshold sets off trains of action potentials, leading to further loses of K+ and Cl-. In final stages of salt damage the H+/OH- channels are thought to become the dominant transporter, dissipating the proton gradient and bringing the cell PD close to 0. The differences in transporter electrophysiology and their synergy under osmotic and/or saline stress in salt sensitive and salt tolerant characean cells are discussed in d
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dual turgor regulation response to hypotonic stress in lamprothamnium papulosum
Plant Cell and Environment, 1999Co-Authors: Mary J Beilby, C A Cherry, Virginia A ShepherdAbstract:Cells of the salt-tolerant charophyte Lamprothamnium respond differently to hypotonic challenge according to their position on the plant (i.e. cell age). Differences in electrophysiological response are coupled with differences in cell fine structure, and the presence or absence of extracellular mucilage. (1) Young, apical (fast-regulating, FR) cells respond with sudden cessation of cyclosis, depolarization to –50 mV (in some cells by more than 100 mV) and increase in Membrane Conductance by up to an order of magnitude. Intracellular [K+]v, [Na+]v and [Cl–]v decrease 1 h after hypotonic challenge. Patch-clamping cytoplasmic droplets reveals two types of K+ channel, 150 pS and 35 pS, and a small Conductance Cl– channel, 35 pS (Conductances at estimated tonoplast resting potential between zero and 20 mV). Extracellular mucilage is thin (< 5 μm thick) or lacking, similar to freshwater Chara. Unlike freshwater charophytes these cells have a canalicular vacuolar system of large surface area and compartment the fluorochrome 6 carboxyfluorescein in the cytoplasm rather than the vacuolar system. (2) Older basal (slow-regulating, SR) cells do not cease streaming on hypotonic challenge and depolarize only slightly (by approximately 20 mV) with small or no change in Membrane Conductance. After 1 h the intracellular [K+]v, [Na+]v and [Cl–]v scarcely change. Patch-clamping cytoplasmic droplets reveals two types of K+ channel, medium Conductance 90 pS and low Conductance (as in FR cells). The large Conductance K+ channel was not observed. The Cl– channel was more active in SR cells. The cells were coated with extracellular mucilage more than 10 μm thick. In a similar manner to freshwater Chara, these cells compartment 6 carboxyfluorescein in a large central vacuole. In the older cells, making up the bulk of any given plant, the simultaneous development of extracellular mucilage and a large central vacuole which compartments 6 carboxyfluorescein is associated with a minimal electrophysiological response to hypotonic challenge. The significance of these findings for salt-tolerance is discussed.
Kathleen A Maguirezeiss - One of the best experts on this subject based on the ideXlab platform.
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α synuclein mediates alterations in Membrane Conductance a potential role for α synuclein oligomers in cell vulnerability
European Journal of Neuroscience, 2010Co-Authors: Li Rebekah Feng, Howard J Federoff, Stefano Vicini, Kathleen A MaguirezeissAbstract:alpha-Synuclein has been linked to the pathogenesis of Parkinson's disease and other synucleinopathies through its propensity to form toxic oligomers. The exact mechanism for oligomeric synuclein-directed cell vulnerability has not been fully elucidated, but one hypothesis portends the formation of synuclein-containing pores within cell Membranes leading to leak channel-mediated calcium influx and subsequent cell death. Here we demonstrate synuclein-induced formation of sodium dodecyl sulfate-stable oligomers, intracellular synuclein-positive aggregates, alterations in Membrane Conductance reminiscent of leak channels and subsequent cytotoxicity in a dopaminergic-like cell line. Furthermore we demonstrate that the synuclein-induced Membrane Conductance changes are blocked by direct extracellular application of an anti-synuclein antibody. The work presented here confirms that synuclein overexpression leads to Membrane Conductance changes and demonstrates for the first time through antibody-blocking studies that synuclein plays a direct role in the formation of leak channels.
