Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells
Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range character...
Ausführliche Beschreibung
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| Autor*in: |
Bogdanov, N. B. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2008 |
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| Schlagwörter: |
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| Anmerkung: |
© Pleiades Publishing, Ltd. 2008 |
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| Übergeordnetes Werk: |
Enthalten in: Biochemistry (Moscow) - Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007, 2(2008), 1 vom: März, Seite 26-32 |
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| Übergeordnetes Werk: |
volume:2 ; year:2008 ; number:1 ; month:03 ; pages:26-32 |
| Links: |
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| DOI / URN: |
10.1007/s11827-008-1005-8 |
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| Katalog-ID: |
SPR022590471 |
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| 100 | 1 | |a Bogdanov, N. B. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
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| 520 | |a Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions | ||
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| 650 | 4 | |a ATPase Activity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Oxygen Partial Pressure |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Ouabain |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Hydrolytic Activity |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Petrushanko, I. Yu. |4 aut | |
| 700 | 1 | |a Boldyrev, A. A. |4 aut | |
| 700 | 1 | |a Gassmann, M. |4 aut | |
| 700 | 1 | |a Bogdanova, A. Yu. |4 aut | |
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10.1007/s11827-008-1005-8 doi (DE-627)SPR022590471 (SPR)s11827-008-1005-8-e DE-627 ger DE-627 rakwb eng Bogdanov, N. B. verfasserin aut Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2008 Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 Petrushanko, I. Yu. aut Boldyrev, A. A. aut Gassmann, M. aut Bogdanova, A. Yu. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 2(2008), 1 vom: März, Seite 26-32 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:2 year:2008 number:1 month:03 pages:26-32 https://dx.doi.org/10.1007/s11827-008-1005-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 2 2008 1 03 26-32 |
| spelling |
10.1007/s11827-008-1005-8 doi (DE-627)SPR022590471 (SPR)s11827-008-1005-8-e DE-627 ger DE-627 rakwb eng Bogdanov, N. B. verfasserin aut Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2008 Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 Petrushanko, I. Yu. aut Boldyrev, A. A. aut Gassmann, M. aut Bogdanova, A. Yu. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 2(2008), 1 vom: März, Seite 26-32 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:2 year:2008 number:1 month:03 pages:26-32 https://dx.doi.org/10.1007/s11827-008-1005-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 2 2008 1 03 26-32 |
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10.1007/s11827-008-1005-8 doi (DE-627)SPR022590471 (SPR)s11827-008-1005-8-e DE-627 ger DE-627 rakwb eng Bogdanov, N. B. verfasserin aut Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2008 Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 Petrushanko, I. Yu. aut Boldyrev, A. A. aut Gassmann, M. aut Bogdanova, A. Yu. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 2(2008), 1 vom: März, Seite 26-32 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:2 year:2008 number:1 month:03 pages:26-32 https://dx.doi.org/10.1007/s11827-008-1005-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 2 2008 1 03 26-32 |
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10.1007/s11827-008-1005-8 doi (DE-627)SPR022590471 (SPR)s11827-008-1005-8-e DE-627 ger DE-627 rakwb eng Bogdanov, N. B. verfasserin aut Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2008 Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 Petrushanko, I. Yu. aut Boldyrev, A. A. aut Gassmann, M. aut Bogdanova, A. Yu. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 2(2008), 1 vom: März, Seite 26-32 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:2 year:2008 number:1 month:03 pages:26-32 https://dx.doi.org/10.1007/s11827-008-1005-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 2 2008 1 03 26-32 |
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10.1007/s11827-008-1005-8 doi (DE-627)SPR022590471 (SPR)s11827-008-1005-8-e DE-627 ger DE-627 rakwb eng Bogdanov, N. B. verfasserin aut Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Pleiades Publishing, Ltd. 2008 Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 Petrushanko, I. Yu. aut Boldyrev, A. A. aut Gassmann, M. aut Bogdanova, A. Yu. aut Enthalten in Biochemistry (Moscow) Dordrecht [u.a.] : Springer Science + Business Media B.V, 2007 2(2008), 1 vom: März, Seite 26-32 (DE-627)546011217 (DE-600)2390072-6 1990-7494 nnns volume:2 year:2008 number:1 month:03 pages:26-32 https://dx.doi.org/10.1007/s11827-008-1005-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 2 2008 1 03 26-32 |
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Enthalten in Biochemistry (Moscow) 2(2008), 1 vom: März, Seite 26-32 volume:2 year:2008 number:1 month:03 pages:26-32 |
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Bogdanov, N. B. @@aut@@ Petrushanko, I. Yu. @@aut@@ Boldyrev, A. A. @@aut@@ Gassmann, M. @@aut@@ Bogdanova, A. Yu. @@aut@@ |
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Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. 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Bogdanov, N. B. |
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Bogdanov, N. B. misc Nitric Oxide misc ATPase Activity misc Oxygen Partial Pressure misc Ouabain misc Hydrolytic Activity Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
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Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells Nitric Oxide (dpeaa)DE-He213 ATPase Activity (dpeaa)DE-He213 Oxygen Partial Pressure (dpeaa)DE-He213 Ouabain (dpeaa)DE-He213 Hydrolytic Activity (dpeaa)DE-He213 |
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Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
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Bogdanov, N. B. Petrushanko, I. Yu. Boldyrev, A. A. Gassmann, M. Bogdanova, A. Yu. |
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Bogdanov, N. B. |
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oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
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Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
| abstract |
Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions © Pleiades Publishing, Ltd. 2008 |
| abstractGer |
Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions © Pleiades Publishing, Ltd. 2008 |
| abstract_unstemmed |
Abstract This study focuses on the oxygen-dependence of active and passive $ K^{+} $ fluxes across membranes of cerebellar granule cells of neonatal rats. Maximal $ Na^{+} $,$ K^{+} $-ATPase activity along with minimal passive $ K^{+} $ influx was observed within oxygen concentration range characteristic for neonatal rat cerebellum. Prolonged exposure to hypoxia as well as hyperoxia resulted in suppression of the $ Na^{+} $,$ K^{+} $-ATPase and activation of the passive $ K^{+} $ flux. Toxic effects of hypoxia could be partially prevented by inhibition of NO production with L-NAME. This was accomplished by suppression of $ Na^{+} $,$ K^{+} $-ATPase with subsequent reduction in ATP consumption concurrently with the reduction in passive $ K^{+} $ flux. Activation of the $ Na^{+} $,$ K^{+} $-ATPase by NO at physiological $ pO_{2} $ could be abolished by inhibition of NO synthase by L-NAME or soluble guanylyl cyclase with ODQ. However, treatment of cells with activator of PKG Rp-8-CTP did not mimic normoxic activation of the active $ K^{+} $ influx. Oxygen-induced responses under normoxic conditions were differentially mediated by α1 isoform of the $ Na^{+} $,$ K^{+} $-ATPase catalytic subunit, whereas α2/3 isoform was predominantly active under conditions of severe hypoxia. We conclude that both hypoxia and hyperoxia trigger a gradual dissipation of transmembrane $ K^{+} $ gradient and loss of excitability of cerebellar neurons. The latter may be partially reversed by suppression of NO production under hypoxic conditions © Pleiades Publishing, Ltd. 2008 |
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Oxygen-sensitivity of potassium fluxes across plasma membrane of cerebellar granule cells |
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Petrushanko, I. Yu Boldyrev, A. A. Gassmann, M. Bogdanova, A. Yu |
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Petrushanko, I. Yu Boldyrev, A. A. Gassmann, M. Bogdanova, A. Yu |
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2024-07-03T13:52:36.659Z |
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|
| score |
7.400079 |