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1.

001-es BibID:BIBFORM064954
Első szerző:Balajthy András (általános orvos)
Cím:7DHC-induced changes of Kv1.3 operation contributes to modified T cell function in Smith-Lemli-Opitz syndrome / András Balajthy, Sándor Somodi, Zoltán Pethő, Mária Péter, Zoltán Varga, Gabriella P. Szabó, György Paragh, László Vígh, György Panyi, Péter Hajdu
Dátum:2016
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 468 : 8 (2016), p. 1403-1418. -
További szerzők:Somodi Sándor (1977-) (belgyógyász) Pethő Zoltán (1989-) (orvos) Péter Mária Varga Zoltán (1969-) (biofizikus, szakfordító) P. Szabó Gabriella (1975-) (csecsemő- és gyermekgyógyász, klinikai genetikus) Paragh György (1953-) (belgyógyász) Vígh László (orvos Szeged) Panyi György (1966-) (biofizikus) Hajdu Péter (1975-) (biofizikus)
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2.

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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3.

001-es BibID:BIBFORM036694
Első szerző:Hegyi Bence (élettanász)
Cím:Tetrodotoxin blocks L-type Ca2+ channels in canine ventricular cardiomyocytes / Bence Hegyi, László Bárándi, István Komáromi, Ferenc Papp, Balázs Horváth, János Magyar, Tamás Bányász, Zoltán Krasznai, Norbert Szentandrássy, Péter P. Nánási
Dátum:2012
ISSN:0031-6768
Megjegyzések:Tetrodotoxin (TTX) is believed to be the mostselective inhibitor of voltage-gated fast Na+ channels inexcitable tissues, including nerve, skeletal muscle, andheart, although TTX sensitivity of the latter is lower thanthe former by at least three orders of magnitude. In thepresent study, the TTX sensitivity of L-type Ca2+ current(ICa) was studied in isolated canine ventricular cells usingconventional voltage clamp and action potential voltageclamp techniques. TTX was found to block ICa in a reversiblemanner without altering inactivation kinetics of ICa.Fitting results to the Hill equation, an IC50 value of55?2 ?M was obtained with a Hill coefficient of unity(1.0?s0.04). The current was fully abolished by 1 ?Mnisoldipine, indicating that it was really ICa. Under actionpotential voltage clamp conditions, the TTX-sensitivecurrent displayed the typical fingerprint of ICa, whichwas absent in the presence of nisoldipine. Stick-and-ballmodels for Cav1.2 and Nav1.5 channel proteins wereconstructed to explain the differences observed betweenaction of TTX on cardiac ICa and INa. This is the firstreport demonstrating TTX to interact with L-type calciumcurrent in the heart.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium channels
Dog heart
Sodium channels
Tetrodotoxin
Voltage clamp
Megjelenés:Pflügers Archiv. - 464 : 2 (2012), p. 167-174. -
További szerzők:Bárándi László (1984-) (élettanász) Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus) Papp Ferenc (1979-) (biofizikus) Horváth Balázs (1981-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Krasznai Zoltán (1950-) (biofizikus) Szentandrássy Norbert (1976-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K100151
OTKA
PD101171
OTKA
K101196
OTKA
CNK-77855
Egyéb
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4.

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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5.

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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6.

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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7.

001-es BibID:BIBFORM057403
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Contribution of ion currents to beat-to-beat variability of action potential duration in canine ventricular myocytes / Norbert Szentandrássy, Kornél Kistamás, Bence Hegyi, Balázs Horváth, Ferenc Ruzsnavszky, Krisztina Váczi, János Magyar, Tamás Bányász, András Varró, Péter P. Nánási
Dátum:2015
ISSN:0031-6768
Megjegyzések:Although beat-to-beat variability (short-term variability, SV) of action potential duration (APD) is considered as a predictor of imminent cardiac arrhythmias, the underlying mechanisms are still not clear. In the present study, therefore, we aimed to determine the role of the major cardiac ion currents, APD, stimulation frequency, and changes in the intracellular Ca2+ concentration ([Ca2+]i) on the magnitude of SV. Action potentials were recorded from isolated canine ventricular cardiomyocytes using conventional microelectrode techniques. SV was an exponential function of APD, when APD was modified by current injections. Drug effects were characterized as relative SV changes by comparing the drug-induced changes in SV to those in APD according to the exponential function obtained with current pulses. Relative SV was increased by dofetilide, HMR 1556, nisoldipine, and veratridine, while it was reduced by BAY K8644, tetrodotoxin, lidocaine, and isoproterenol. Relative SV was also increased by increasing the stimulation frequency and [Ca2+]i. In summary, relative SV is decreased by ion currents involved in the negative feedback regulation of APD (I Ca, I Ks, and I Kr), while it is increased by I Na and I to. We conclude that drug-induced effects on SV should be evaluated in relation with the concomitant changes in APD. Since relative SV was decreased by ion currents playing critical role in the negative feedback regulation of APD, blockade of these currents, or the beta-adrenergic pathway, may carry also some additional proarrhythmic risk in addition to their well-known antiarrhythmic action.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Short-term variability
Action potential duration
Ion currents
Canine myocytes
Action potential configuration
Doktori iskola
Megjelenés:Pflügers Archiv. - 467 : 7 (2015), p. 1431-1443. -
További szerzők:Kistamás Kornél (1986-) (biológus) Hegyi Bence (1987-) (élettanász) Horváth Balázs (1981-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Váczi Krisztina (1987-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K10015
OTKA
K109736
OTKA
K101196
OTKA
PD101171
OTKA
NK104331
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Élettan Kutatócsoport
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
TÁMOP-4.2.4.A/2-11/1- 2012-0001
TÁMOP
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8.

001-es BibID:BIBFORM043347
035-os BibID:PMID:23553419
Első szerző:Szilágyi Orsolya (molekuláris biológus, biokémikus)
Cím:The role of PSD-95 in the rearrangement of Kv1.3 channels to the immunological synapse / Orsolya Szilágyi, Anita Boratkó, György Panyi, Péter Hajdu
Dátum:2013
ISSN:0031-6768
Megjegyzések:Establishment of the immunological synapse (IS) between T lymphocytes and antigen-presenting cells is a key step in the adaptive immune response. Several proteins accumulate in the IS, such as the Kv1.3 potassium channel; however, the mechanism of this translocation is unknown. PSD-95 and SAP97 are adaptor proteins that regulate the polarized cell surface expression and localization of Kv1 channels in neurons. We investigated whether these proteins affect the redistribution of Kv1.3 into the IS in non-excitable human T cells. We show here that PSD-95 and SAP97 are expressed in Jurkat and interact with the C terminus of Kv1.3. Disruption of the interaction between PSD-95 or SAP97 and Kv1.3 in Jurkat was realized by the expression of a C-terminal truncated Kv1.3, which lacks the binding domain for these proteins, or by the knockdown of the expression of PSD-95 or SAP97 using specific shRNA. Expression of the truncated Kv1.3 or knockdown of PSD-95, but not the knockdown of SAP97, inhibited the recruitment of Kv1.3 into the IS; the fraction of cells showing polarized Kv1.3 expression upon engagement in an IS was significantly lower than in control cells expressing the full-length Kv1.3, and the rearrangement of Kv1.3 did not show time dependence. In contrast, Jurkat cells expressing the full-length channel showed marked time dependence in the recruitment into the IS peaking at 1 min after the conjugation of the cells. These results demonstrate that PSD-95 participates in the targeting of Kv1.3 into the IS, implying its important role in human T-cell activation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Doktori iskola
Megjelenés:Pflugers Archiv-European Journal of Physiology. - 465 : 9 (2013), p. 1341-1353. -
További szerzők:Boratkó Anita (1985-) (biokémikus, molekuláris biológus) Panyi György (1966-) (biofizikus) Hajdu Péter (1975-) (biofizikus)
Pályázati támogatás:TÁMOP-4.2.2-A-11/1/KONV-2012-0025
TÁMOP
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
TÁMOP-4.2.2-08/1-2008-0019
TÁMOP
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9.

001-es BibID:BIBFORM050561
035-os BibID:PMID:24114173
Első szerző:Varga Angelika (biológus)
Cím:Anandamide produced by Ca2+-insensitive enzymes induces excitation in primary sensory neurons / Angelika Varga, Agnes Jenes, Timothy H. Marczylo, Joao Sousa-Valente, Jie Chen, Jonothan Austin, Srikumaran Selvarajah, Fabiana Piscitelli, Anna P. Andreou, Anthony H. Taylor, Fiona Kyle, Mohammed Yaqoob, Sue Brain, John P. M. White, Laszlo Csernoch, Vincenzo Di Marzo, Laki Buluwela, Istvan Nagy
Dátum:2014
ISSN:0031-6768
Megjegyzések:The endogenous lipid agent N-arachidonoylethanolamine (anandamide), among other effects, has been shown to be involved in nociceptive processing both in the central and peripheral nervous systems. Anandamide is thought to be synthesised by several enzymatic pathways both in a Ca2+-sensitive and Ca2+-insensitive manner, and rat primary sensory neurons produce anandamide. Here, we show for the first time, that cultured rat primary sensory neurons express at least four of the five known Ca2+-insensitive enzymes implicated in the synthesis of anandamide, and that application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl, the common substrate of the anandamide-synthesising pathways, results in anandamide production which is not changed by the removal of extracellular Ca2+. We also show that anandamide, which has been synthesised in primary sensory neurons following the application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl induces a transient receptor potential vanilloid type 1 ion channel-mediated excitatory effect that is not inhibited by concomitant activation of the cannabinoid type 1 receptor. Finally, we show that sub-populations of transient receptor potential vanilloid type 1 ion channel-expressing primary sensory neurons also express some of the putative Ca2+-insensitive anandamide-synthesising enzymes. Together, these findings indicate that anandamide synthesised by primary sensory neuron via a Ca2+-insensitive manner has an excitatory rather than an inhibitory role in primary sensory neurons and that excitation is mediated predominantly through autocrine signalling. Regulation of the activity of the Ca2+-insensitive anandamide-synthesising enzymes in these neurons may be capable of regulating the activity of these cells, with potential relevance to controlling nociceptive processing.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflugers Archiv. - 466 : 7 (2014), p. 1421-1435. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Marczylo, Timothy H. Sousa-Valente, Joao Chen, Jie Austin, Jonothan Selvarajah, Srikumaran Piscitelli, Fabiana Andreou, Anna P. Taylor, Anthony H. Kyle, Fiona Yaqoob, Mohammed Brain, Sue White, John P. M. Csernoch László (1961-) (élettanász) Di Marzo, Vincenzo Buluwela, Laki Nagy István
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