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1.

001-es BibID:BIBFORM004134
Első szerző:Almássy János (élettanász, biológus, angol-magyar szakfordító)
Cím:Effects of K-201 on the calcium pump and calcium release channel of rat skeletal muscle / Janos Almassy, Monika Sztretye, Balazs Lukacs, Beatrix Dienes, Laszlo Szabo, Peter Szentesi, Guy Vassort, Laszlo Csernoch, Istvan Jona
Dátum:2008
ISSN:0031-6768
Megjegyzések:The benzothiazepine derivative K-201 has been suggested as a potential therapeutic agent due to its antiarrhythmogenic action. To understand how the drug alters calcium release from the sarcoplasmic reticulum (SR), we investigated its effects on the SR calcium channel and calcium pump by single channel electrophysiology, whole-cell confocal microscopy, and ATPase activity measurements on control and post-myocardial infarcted (PMI) rat skeletal muscle. In bilayers, K-201 induced two subconductance states corresponding to approximately 24% (S(1)) and approximately 13% (S(2)) of the maximum conductance. Dependence of event frequency and of time spent in S(1) and S(2) on the drug concentration was biphasic both in control and in PMI rats, with a maximum at 50 microM. At this concentration, the channel spends 26 +/- 4% and 24 +/- 4%, respectively, of the total time in these subconductance states at positive potentials, while no subconductances are observed at negative potentials. K-201 altered the frequency of elementary calcium release events: spark frequency decreased from 0.039 +/- 0.001 to 0.023 +/- 0.001 s(-1) sarcomere(-1), while the frequency of embers increased from 0.011 +/- 0.001 to 0.023 +/- 0.001 s(-1) sarcomere(-1). Embers with different amplitude levels were observed after the addition of the drug. K-201 inhibited the Ca(2+) ATPase characterized by IC(50,contr) = 119 +/- 21 muM and n (Hill,contr) = 1.84 +/- 0.48 for control and IC(50,PMI) = 122 +/- 18 microM and n (Hill,PMI) = 1.97 +/- 0.24 for PMI animals. These results suggest that although K-201 would increase the appearance of subconductance states, the overall calcium release is reduced by the drug. In addition, the effect of K-201 is identical on calcium release channels from control and PMI rats.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 457 : 1 (2008), p. 171-183. -
További szerzők:Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Lukács Balázs (1978-) (élettanász) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Szabó László (Románia) Szentesi Péter (1967-) (élettanász) Vassort, Guy Csernoch László (1961-) (élettanász) Jóna István (1948-) (élettanász, fizikus)
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2.

001-es BibID:BIBFORM040112
Első szerző:Collet, Claude
Cím:Effects of extracellular ATP on freshly isolated mouse skeletal muscle cells during pre-natal and post-natal development / Collet Claude, Strube Caroline, Csernoch Laszlo, Mallouk Nora, Ojeda Carlos, Allard Bruno, Jacquemond Vincent
Dátum:2002
ISSN:0031-6768
Megjegyzések:Extracellular adenosine 5'-triphosphate (ATP) has profound effects on membrane conductance and on the intracellular free [Ca(2+)] ([Ca(2+)](i)) in cultured skeletal muscle cells. The aim of the present study was to examine the occurrence and to characterize the properties of such responses during mammalian muscle development in vivo. The effect of ATP (0.2 mM) was tested on membrane current and [Ca(2+)](i) in freshly isolated pre- and post-natal mouse skeletal muscle cells. Pre-natal cells were from 14- to 19-day-old fetuses. In pre- and early post-natal cells, very small elevations of [Ca(2+)](i) (<50 nM) following ATP application could be detected with the fluorescent indicator fura-2. A clear subsarcolemmal rise in [Ca(2+)] was however associated to the presence of ATP, as demonstrated by increased activity of plasma membrane Ca(2+)-activated K(+) channels in cells bathed in a depolarizing, high-calcium-containing solution. In cells voltage-clamped at -80 mV in external Tyrode, ATP induced an inward current associated with an increased membrane conductance. The mean maximal amplitude of the ATP-induced current was -0.84 +/- 0.07 A/F ( n=39). The response to ATP was still present after birth, although its amplitude tended to decrease with post-natal development and was completely absent in muscle cells from 3- to 6-month-old mice. The ATP-induced current could be abolished reversibly by suramin. Our results suggest that, over the range of developmental stages examined, skeletal muscle cells display an ionotropic purinergic signalling pathway with functional properties qualitatively consistent with what is observed in cultured myotubes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 443 : 5-6 (2002), p. 771-778. -
További szerzők:Strube, Caroline Csernoch László (1961-) (élettanász) Mallouk, Nora Ojeda, Carlos Allard, Bruno Jacquemond, Vincent
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3.

001-es BibID:BIBFORM004135
Első szerző:Cseri Julianna (laboratóriumi diagnosztika szakorvos)
Cím:A purinergic signal transduction pathway in mammalian skeletal muscle cells in culture / Julianna Cseri, Henrietta Szappanos, Gyula Péter Szigeti, Zoltán Csernátony, László Kovács, László Csernoch
Dátum:2002
ISSN:0031-6768
Megjegyzések:The effects of adenosine 5'-triphosphate (ATP) on human and mouse skeletal muscle fibres in primary culture were investigated. ATP-evoked changes in intracellular calcium concentration ([Ca(2+)](i)) were measured and compared with those induced by agonists of the nicotinic acetylcholine (Ach)- and P2X purinoreceptors. While ATP was effective on both myoblasts and multi-nucleated myotubes in the micromolar range, Ach failed to induce any change in [Ca(2+)](i) at early stages of development. In contrast, myofibres with peripheral nuclei showed little response to ATP but responded to Ach with a large change in [Ca(2+)](i). The responsiveness of the myotubes to Ach paralleled that to potassium. The removal of external calcium abolished the response to ATP. P2X receptor agonists mimicked the response to ATP with the order of potency being ATP>2',3'- O-(4-benzoyl)-benzoyl-ATP>beta,gamma-methylene-ATP>alpha,beta-methylene-ATP. Under voltage-clamp conditions ATP induced an inward current that showed little inactivation. These results are consistent with the existence of P2X receptor-mediated signal transduction pathway in cultured mammalian skeletal muscle cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 443 : 5-6 (2002), p. 731-738. -
További szerzők:Szappanos Henrietta (1976-) (biológus, élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Csernátony Zoltán (1959-2023) (ortopéd sebész, traumatológus) Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász)
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4.

001-es BibID:BIBFORM001079
Első szerző:Csernoch László (élettanász)
Cím:Sparks and embers of skeletal muscle : the exciting events of contractile activation / László Csernoch
Dátum:2007
ISSN:0031-6768
Megjegyzések:Intracellular calcium concentration ([Ca(2+)](i)) is a key player in a wide range of cellular functions from long-term effects that determine the fate of the cell to immediate responses as secretion and motility. To initiate contraction, calcium ions in skeletal muscle are released into the myoplasm through the calcium channels, the ryanodine receptors, of the sarcoplasmic reticulum. The opening of these channels give rise to localised increases in [Ca(2+)](i), originally termed calcium sparks, that fuse and generate the global calcium transient. Whereas calcium sparks in amphibians are abundant and stereotyped, events in mammalian skeletal muscle are scarce and morphologically diverse. This review compares the different forms of calcium release events, occurring spontaneously or evoked by a depolarising pulse, observed in the different classes of vertebrates. It then addresses the questions whether or not these events can be considered as elementary and how the global calcium transient can be reconstructed from them.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 454 : 6 (2007), p. 869-878. -
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5.

001-es BibID:bibEBI00019167
Első szerző:Deli Tamás (szülész-nőgyógyász, endokrinológus szakorvos)
Cím:Contribution from P2X and P2Y purinoreceptors to ATP-evoked changes in intracellular calcium concentration on cultured myotubes / Tamás Deli, Henrietta Szappanos, Gyula Péter Szigeti, Julianna Cseri, László Kovács, László Csernoch
Dátum:2007
ISSN:0031-6768
Megjegyzések:Although the alteration of purinoreceptor pattern on skeletal muscle is known to accompany physiological muscle differentiation and the pathogenesis of muscle dystrophy, the exact identity of and the relative contribution from the individual receptor subtypes to the purinergic signal have been controversial. To identify these subtypes in cultured myotubes of 5-10 nuclei, changes in intracellular calcium concentration and surface membrane ionic currents were detected and calcium fluxes calculated after the application of the subtype-specific agonists 2'3'-O-(benzoyl-4-benzoyl)-ATP (BzATP), 2-methyltio-ADP and UTP. The effectiveness of these agonists together with positive immunocytochemical staining revealed the presence of P2X(4), P2X(5), P2X(7), P2Y(1) and P2Y(4) receptors. siRNA-reduced protein expression of P2X(5), P2X(7) and P2Y(1) receptors was accompanied by reduction in the ATP-evoked calcium transients. Furthermore, anti-P2X(7) siRNA caused a significant drop in the early peak and delayed steady component of the calculated calcium flux. The use of its antagonist, oxidized ATP, similarly to transfection with anti-P2X(7) siRNA caused significant reduction in the agonist-elicited ionic currents I (ATP) and I (BzATP), with a greater drop in the latter. Our results demonstrate that the activation of ionotropic P2X(4), P2X(5) and P2X(7) and metabotropic P2Y(1) and P2Y(4) purinoreceptors participates in forming the calcium transients of multinucleated myotubes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 453 : 4 (2007), p. 519-529. -
További szerzők:Szappanos Henrietta (1976-) (biológus, élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász)
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6.

001-es BibID:BIBFORM057717
Első szerző:González Rodríguez, Estela
Cím:Phosphoinositide substrates of myotubularin affect voltage-activated Ca2+ release in skeletal muscle / Estela González Rodríguez, Romain Lefebvre, Dóra Bodnár, Claude Legrand, Peter Szentesi, János Vincze, Karine Poulard, Justine Bertrand-Michel, Laszlo Csernoch, Anna Buj-Bello, Vincent Jacquemond
Dátum:2014
ISSN:0031-6768
Megjegyzések:Skeletal muscle excitation?contraction (E?C) couplingis altered in several models of phosphatidylinositol phosphate(PtdInsP) phosphatase deficiency and ryanodine receptoractivity measured in vitro was reported to be affected by certainPtdInsPs, thus prompting investigation of the physiologicalrole of PtdInsPs in E?C coupling. We measured intracellularCa2+ transients in voltage-clamped mouse muscle fibresmicroinjected with a solution containing a PtdInsP substrate(PtdIns(3,5)P2 or PtdIns(3)P) or product (PtdIns(5)P orPtdIns) of the myotubularin phosphatase MTM1. No significantchange was observed in the presence of either PtdIns(5)Por PtdIns but peak SR Ca2+ release was depressed by ~30%and50% in fibres injected with PtdIns(3,5)P2 and PtdIns(3)P,respectively, with no concurrent alteration in the membranecurrent signals associated with the DHPR function as well asin the voltage dependence of Ca2+ release inactivation. Inpermeabilized muscle fibres, the frequency of spontaneousCa2+ release events was depressed in the presence of the threetested phosphorylated forms of PtdInsP with PtdIns(3,5)P2being the most effective, leading to an almost complete disappearanceof Ca2+ release events. Results support the possibilitythat pathological accumulation of MTM1 substrates mayacutely depress ryanodine receptor-mediated Ca2+ release.Overexpression of a mCherry-tagged form of MTM1 in musclefibres revealed a striated pattern consistent with the triadicarea. Ca2+ release remained although unaffected by MTM1overexpression and was also unaffected by the PtdIns-3-kinaseinhibitor LY2940002, suggesting that the 3-phosphorylatedPtdIns lipids active on voltage-activated Ca2+ release are inherentlymaintained at a low level, inefficient on Ca2+ releasein normal conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium homeostasis
Excitation-contraction coupling
Ryanodine receptor
Sarcoplasmic reticulum Ca2+ release
Phosphatidylinositol phosphate
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 466 : 5 (2014), p. 973-985. -
További szerzők:Lefebvre, Romain Bodnár Dóra (1987-) (molekuláris biológus) Legrand, Claude Szentesi Péter (1967-) (élettanász) Vincze János (1988-) (orvos) Poulard, Karine Bertrand-Michel, Justine Csernoch László (1961-) (élettanász) Buj-Bello, Anna Jacquemond, Vincent
Pályázati támogatás:OTKA-K107765
OTKA
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7.

001-es BibID:BIBFORM039994
Első szerző:Jóna István (élettanász, fizikus)
Cím:Altered inhibition of the rat skeletal ryanodine receptor/calcium release channel by magnesium in the presence of ATP / I. Jóna, C. Szegedi, S. Sárközi, P. Szentesi, L. Csernoch, L. Kovács
Dátum:2001
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv. - 441 : 6 (2001), p. 729-738. -
További szerzők:Szegedi Csaba Sárközi Sándor (1966-) (élettanász) Szentesi Péter (1967-) (élettanász) Csernoch László (1961-) (élettanász) Kovács László (1939-) (élettanász)
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8.

001-es BibID:BIBFORM037816
Első szerző:Kőszeghy Áron (Ph.D hallgató, élettanász)
Cím:Activation of muscarinic receptors increases the activity of the granule neurones of the rat dorsal cochlear nucleus : a calcium imaging study / Áron Kőszeghy, János Vincze, Zoltán Rusznák, Yuhong Fu, George Paxinos, László Csernoch, Géza Szücs
Dátum:2012
ISSN:0031-6768
Megjegyzések:Acetylcholine modulates the function of the cochlear nucleus via several pathways. In this study the effects of cholinergic stimulation were studied on the cytoplasmic Ca2+ concentration of granule neurones of the rat dorsal cochlear nucleus (DCN). Ca2+ transients were recorded in Oregon-Green-BAPTA 1-loaded brain slices using a calcium imaging technique. For the detection, identification, and characterisation of the Ca2+ transients, a wavelet analysis-based method was developed. Granule cells were identified on the basis of their size and localisation. The action potential-coupled character of the Ca2+ transients of the granule cells was established by recording fluorescence changes and electrical activity simultaneously. Application of the cholinergic agonist carbamyl-choline (CCh) significantly increased the frequency of the Ca2+ transients (from 0.37 to 6.31 min-1, corresponding to a 17.1-fold increase; n = 89). This effect was antagonised by atropine, whereas CCh could still evoke an 8.3-fold increase of the frequency of the Ca2+ transients when hexamethonium was present. Using immunolabelling, the expression of both type 1 and type 3 muscarinic receptors (M1 and M3 receptors, respectively) was demonstrated in the granule cells. Application of 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (an M3-specific antagonist) prevented the onset of the CCh effect, whereas an M1-specific antagonist (pirenzepine) was less effective. We conclude that cholinergic stimulation increases the activity of granule cells, mainly by acting on their M3 receptors. The modulation of the firing activity of the granule cells, in turn, may modify the firing of projection neurones, and may adjust signal processing in the entire DCN.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 463 : 6 (2012), p. 829-844. -
További szerzők:Vincze János (1988-) (orvos) Rusznák Zoltán (1965-) (élettanász) Fu, YuHong Paxinos, George Csernoch László (1961-) (élettanász) Szűcs Géza (1948-) (élettanász)
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9.

001-es BibID:BIBFORM053082
Első szerző:Matta Csaba (molekuláris biológus, genetikus, angol szakfordító)
Cím:Purinergic signalling is required for calcium oscillations in migratory chondrogenic progenitor cells / Csaba Matta, János Fodor, Nicolai Miosge, Roland Takács, Tamás Juhász, Henrik Rybaltovszki, Adrienn Tóth, László Csernoch, Róza Zákány
Dátum:2015
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Doktori iskola
Megjelenés:Pflugers Archiv-European Journal Of Physiology 467 : 2 (2015), p. 429-442. -
További szerzők:Fodor János (1973-) (élettanász, biotechnológus) Miosge, Nicolai Takács Roland Ádám (1985-) (molekuláris biológus, biokémikus) Juhász Tamás (1976-) (biológus, orvosbiológus) Rybaltovszki Henrik (1973-) (ortopéd és baleseti sebész, traumatológus) Tóth Adrienn (1988-) (molekuláris biológus, élettanász) Csernoch László (1961-) (élettanász) Zákány Róza (1963-) (anatómus-, kötőszövetbiológus)
Pályázati támogatás:CNK-80709
OTKA
NN-107765
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0036
TÁMOP
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Idegtudományi Doktori Iskola
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10.

001-es BibID:BIBFORM018361
Első szerző:Oláh Tamás (élettanász)
Cím:Trisk 32 regulates IP3 receptors in rat skeletal myoblasts / Oláh Tamás, Fodor János, Oddoux Sarah, Ruzsnavszky Olga, Marty Isabelle, Csernoch László
Dátum:2011
ISSN:0031-6768
Megjegyzések:To date, four isoforms of triadins have been identified in rat skeletal muscle. While the function of the 95-kDa isoform in excitation-contraction coupling has been studied in detail, the role of the 32-kDa isoform (Trisk 32) remains elusive. Here, Trisk 32 overexpression was carried out by stable transfection in L6.G8 myoblasts. Co-localization of Trisk 32 and IP(3) receptors (IP(3)R) was demonstrated by immunocytochemistry, and their association was shown by co-immunoprecipitation. Functional effects of Trisk 32 on IP(3)-mediated Ca(2+) release were assessed by measuring changes in [Ca(2+)](i) following the stimulation by bradykinin or vasopressin. The amplitude of the Ca(2+) transients evoked by 20 mikroM bradykinin was significantly higher in Trisk 32-overexpressing (p<0.01; 426 ±84 nM, n=27) as compared to control cells (76±12 nM, n=23). The difference remained significant (p<0.02; 217±41 nM, n=21, and 97±29 nM, n=31, respectively) in the absence of extracellular Ca(2+). Similar observations were made when 0.1 mikroM vasopressin was used to initiate Ca(2+) release. Possible involvement of the ryanodine receptors (RyR) in these processes was excluded, after functional and biochemical experiments. Furthermore, Trisk 32 overexpression had no effect on store-operated Ca(2+) entry, despite a decrease in the expression of STIM1. These results suggest that neither the increased activity of RyR, nor the amplification of SOCE, is responsible for the differences observed in bradykinin- or vasopressin-evoked Ca(2+) transients; rather, they were due to the enhanced activity of IP(3)R. Thus, Trisk 32 not only co-localizes with, but directly contributes to, the regulation of Ca(2+) release via IP(3)R.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Inositol 1,4,5-trisphosphate
Skeletal muscle
Myoblasts
Calcium transient
Endoplasmic reticulum
Megjelenés:Pflügers Archiv. - 462 : 4 (2011), p. 599-610. -
További szerzők:Fodor János (1973-) (élettanász, biotechnológus) Oddoux, Sarah Ruzsnavszky Olga (1983-) (élettanász) Marty, Isabelle Csernoch László (1961-) (élettanász)
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11.

001-es BibID:BIBFORM001402
Első szerző:Szigeti Gyula (élettanász, elektrofiziológus)
Cím:Differentiation-dependent alterations in the extracellular ATP-evoked calcium fluxes of cultured skeletal muscle cells from mice / Gyula Péter Szigeti, Henrietta Szappanos, Tamás Deli, Julianna Cseri, László Kovács, László Csernoch
Dátum:2007
ISSN:0031-6768
Megjegyzések:Although extracellular adenosine triphosphate (ATP) has been generally accepted as the regulator of cellular differentiation, the relative contribution of the various purinoreceptor subtypes to purinergic signalling at distinct stages of skeletal muscle differentiation is still poorly understood. Here we measured extracellular ATP-evoked changes in intracellular calcium concentration and surface membrane ionic currents (I (ATP)), calculated the calcium flux (FL) entering the myoplasmic space and compared these parameters at different stages of differentiation on cultured mouse myotubes. The ATP-evoked FL displayed an early peak and then declined to a steady level. With differentiation, the early peak became separated from the maintained component and was absent on mature myotubes. Repeated ATP applications caused desensitization of the response in both immature and differentiated myotubes, owing mainly to the reduction of the early peak of FL in the former and to a decline of both components in the latter group of cells. Depolarization of the cell or removal of external calcium suppressed the early peak. I (ATP) showed no inactivation, and its voltage dependence displayed strong inward rectification. The concentration dependence of I (ATP) can be fitted using a Hill equation, yielding an EC(50) of 56 microM. Results are consistent with the parallel activation of both P2X and P2Y receptors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 453 : 4 (2007), p. 509-518. -
További szerzők:Deli Tamás (1979-) (szülész-nőgyógyász, endokrinológus szakorvos) Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Kovács László (1939-) (élettanász) Csernoch László (1961-) (élettanász) Szappanos Henrietta (1976-) (biológus, élettanász)
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12.

001-es BibID:BIBFORM001082
Első szerző:Szigeti Gyula (élettanász, elektrofiziológus)
Cím:Alterations in the calcium homeostasis of skeletal muscle from postmyocardial infarcted rats / Gyula Péter Szigeti, János Almássy, Mónika Sztretye, Beatrix Dienes, László Szabó, Péter Szentesi, Guy Vassort, Sándor Sárközi, László Csernoch, István Jóna
Dátum:2007
ISSN:0031-6768
Megjegyzések:In chronic heart failure, skeletal muscles develop a weakness that is not associated to an impaired circulatory function but rather to alterations in the skeletal muscle fibers themselves. To understand these changes, the steps in excitation-contraction coupling of rats that underwent a left anterior coronary artery occlusion were studied. About 24 weeks after the myocardial infarction, neither the total amount nor the voltage dependence of intramembrane charge were altered. In contrast, calcium release from the sarcoplasmic reticulum was considerably suppressed, and its voltage dependence shifted toward more positive voltages. Elementary calcium-release events showed altered morphology as the relative proportion of embers increased. Calcium sparks were smaller in amplitude and had larger time-to-peak values. Isolated ryanodine receptors (RyR) displayed an unusual rectification with increased single-channel conductance at positive (cis vs trans) voltages. In addition, the bell-shaped calcium dependence of channel activity was broader, with a slight shift of activation to lower and a larger shift in inactivation to higher calcium concentrations. These data indicate that the number of channels that open during a calcium-release event is decreased and that RyR function is altered; thus, calcium-release is suppressed after a myocardial infarction. These observations give an explanation for the impaired skeletal muscle function in these animals.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 455 : 3 (2007), p. 541-553. -
További szerzők:Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Sztretye Mónika (1981-) (élettanász, elektrofiziológus) Dienes Beatrix (1972-) (élettanász, molekuláris biológus) Szabó László (orvos) Szentesi Péter (1967-) (élettanász) Vassort, Guy Sárközi Sándor (1966-) (élettanász) Csernoch László (1961-) (élettanász) Jóna István (1948-) (élettanász, fizikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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