Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9)
Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome followi...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Ehling, Petra [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2010 |
|---|
| Schlagwörter: |
|---|
| Anmerkung: |
© Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
|---|
| Übergeordnetes Werk: |
Enthalten in: Experimental & translational stroke medicine - London : BioMed Central, 2009, 2(2010), 1 vom: 20. Juli |
|---|---|
| Übergeordnetes Werk: |
volume:2 ; year:2010 ; number:1 ; day:20 ; month:07 |
| Links: |
|---|
| DOI / URN: |
10.1186/2040-7378-2-14 |
|---|
| Katalog-ID: |
SPR030951070 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | SPR030951070 | ||
| 003 | DE-627 | ||
| 005 | 20230519124616.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 201007s2010 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1186/2040-7378-2-14 |2 doi | |
| 035 | |a (DE-627)SPR030951070 | ||
| 035 | |a (SPR)2040-7378-2-14-e | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Ehling, Petra |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| 264 | 1 | |c 2010 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( | ||
| 520 | |a Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. | ||
| 650 | 4 | |a Cerebral Ischemia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Middle Cerebral Artery Occlusion |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Infarct Volume |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Wildtype Mouse |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Transient Middle Cerebral Artery Occlusion |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Bittner, Stefan |4 aut | |
| 700 | 1 | |a Bobak, Nicole |4 aut | |
| 700 | 1 | |a Schwarz, Tobias |4 aut | |
| 700 | 1 | |a Wiendl, Heinz |4 aut | |
| 700 | 1 | |a Budde, Thomas |4 aut | |
| 700 | 1 | |a Kleinschnitz, Christoph |4 aut | |
| 700 | 1 | |a Meuth, Sven G |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Experimental & translational stroke medicine |d London : BioMed Central, 2009 |g 2(2010), 1 vom: 20. Juli |w (DE-627)611727404 |w (DE-600)2520967-X |x 2040-7378 |7 nnns |
| 773 | 1 | 8 | |g volume:2 |g year:2010 |g number:1 |g day:20 |g month:07 |
| 856 | 4 | 0 | |u https://dx.doi.org/10.1186/2040-7378-2-14 |z kostenfrei |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a SYSFLAG_A | ||
| 912 | |a GBV_SPRINGER | ||
| 912 | |a SSG-OLC-PHA | ||
| 912 | |a GBV_ILN_11 | ||
| 912 | |a GBV_ILN_20 | ||
| 912 | |a GBV_ILN_22 | ||
| 912 | |a GBV_ILN_23 | ||
| 912 | |a GBV_ILN_24 | ||
| 912 | |a GBV_ILN_39 | ||
| 912 | |a GBV_ILN_40 | ||
| 912 | |a GBV_ILN_60 | ||
| 912 | |a GBV_ILN_62 | ||
| 912 | |a GBV_ILN_63 | ||
| 912 | |a GBV_ILN_65 | ||
| 912 | |a GBV_ILN_69 | ||
| 912 | |a GBV_ILN_73 | ||
| 912 | |a GBV_ILN_74 | ||
| 912 | |a GBV_ILN_95 | ||
| 912 | |a GBV_ILN_105 | ||
| 912 | |a GBV_ILN_110 | ||
| 912 | |a GBV_ILN_151 | ||
| 912 | |a GBV_ILN_161 | ||
| 912 | |a GBV_ILN_170 | ||
| 912 | |a GBV_ILN_206 | ||
| 912 | |a GBV_ILN_213 | ||
| 912 | |a GBV_ILN_230 | ||
| 912 | |a GBV_ILN_285 | ||
| 912 | |a GBV_ILN_293 | ||
| 912 | |a GBV_ILN_602 | ||
| 912 | |a GBV_ILN_2003 | ||
| 912 | |a GBV_ILN_2005 | ||
| 912 | |a GBV_ILN_2009 | ||
| 912 | |a GBV_ILN_2011 | ||
| 912 | |a GBV_ILN_2014 | ||
| 912 | |a GBV_ILN_2055 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_4012 | ||
| 912 | |a GBV_ILN_4037 | ||
| 912 | |a GBV_ILN_4112 | ||
| 912 | |a GBV_ILN_4125 | ||
| 912 | |a GBV_ILN_4126 | ||
| 912 | |a GBV_ILN_4249 | ||
| 912 | |a GBV_ILN_4305 | ||
| 912 | |a GBV_ILN_4306 | ||
| 912 | |a GBV_ILN_4307 | ||
| 912 | |a GBV_ILN_4313 | ||
| 912 | |a GBV_ILN_4322 | ||
| 912 | |a GBV_ILN_4323 | ||
| 912 | |a GBV_ILN_4324 | ||
| 912 | |a GBV_ILN_4325 | ||
| 912 | |a GBV_ILN_4338 | ||
| 912 | |a GBV_ILN_4367 | ||
| 912 | |a GBV_ILN_4700 | ||
| 951 | |a AR | ||
| 952 | |d 2 |j 2010 |e 1 |b 20 |c 07 | ||
| author_variant |
p e pe s b sb n b nb t s ts h w hw t b tb c k ck s g m sg sgm |
|---|---|
| matchkey_str |
article:20407378:2010----::wprdmiptsimhnesneerlshmafcs |
| hierarchy_sort_str |
2010 |
| publishDate |
2010 |
| allfields |
10.1186/2040-7378-2-14 doi (DE-627)SPR030951070 (SPR)2040-7378-2-14-e DE-627 ger DE-627 rakwb eng Ehling, Petra verfasserin aut Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Bittner, Stefan aut Bobak, Nicole aut Schwarz, Tobias aut Wiendl, Heinz aut Budde, Thomas aut Kleinschnitz, Christoph aut Meuth, Sven G aut Enthalten in Experimental & translational stroke medicine London : BioMed Central, 2009 2(2010), 1 vom: 20. Juli (DE-627)611727404 (DE-600)2520967-X 2040-7378 nnns volume:2 year:2010 number:1 day:20 month:07 https://dx.doi.org/10.1186/2040-7378-2-14 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2010 1 20 07 |
| spelling |
10.1186/2040-7378-2-14 doi (DE-627)SPR030951070 (SPR)2040-7378-2-14-e DE-627 ger DE-627 rakwb eng Ehling, Petra verfasserin aut Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Bittner, Stefan aut Bobak, Nicole aut Schwarz, Tobias aut Wiendl, Heinz aut Budde, Thomas aut Kleinschnitz, Christoph aut Meuth, Sven G aut Enthalten in Experimental & translational stroke medicine London : BioMed Central, 2009 2(2010), 1 vom: 20. Juli (DE-627)611727404 (DE-600)2520967-X 2040-7378 nnns volume:2 year:2010 number:1 day:20 month:07 https://dx.doi.org/10.1186/2040-7378-2-14 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2010 1 20 07 |
| allfields_unstemmed |
10.1186/2040-7378-2-14 doi (DE-627)SPR030951070 (SPR)2040-7378-2-14-e DE-627 ger DE-627 rakwb eng Ehling, Petra verfasserin aut Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Bittner, Stefan aut Bobak, Nicole aut Schwarz, Tobias aut Wiendl, Heinz aut Budde, Thomas aut Kleinschnitz, Christoph aut Meuth, Sven G aut Enthalten in Experimental & translational stroke medicine London : BioMed Central, 2009 2(2010), 1 vom: 20. Juli (DE-627)611727404 (DE-600)2520967-X 2040-7378 nnns volume:2 year:2010 number:1 day:20 month:07 https://dx.doi.org/10.1186/2040-7378-2-14 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2010 1 20 07 |
| allfieldsGer |
10.1186/2040-7378-2-14 doi (DE-627)SPR030951070 (SPR)2040-7378-2-14-e DE-627 ger DE-627 rakwb eng Ehling, Petra verfasserin aut Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Bittner, Stefan aut Bobak, Nicole aut Schwarz, Tobias aut Wiendl, Heinz aut Budde, Thomas aut Kleinschnitz, Christoph aut Meuth, Sven G aut Enthalten in Experimental & translational stroke medicine London : BioMed Central, 2009 2(2010), 1 vom: 20. Juli (DE-627)611727404 (DE-600)2520967-X 2040-7378 nnns volume:2 year:2010 number:1 day:20 month:07 https://dx.doi.org/10.1186/2040-7378-2-14 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2010 1 20 07 |
| allfieldsSound |
10.1186/2040-7378-2-14 doi (DE-627)SPR030951070 (SPR)2040-7378-2-14-e DE-627 ger DE-627 rakwb eng Ehling, Petra verfasserin aut Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Bittner, Stefan aut Bobak, Nicole aut Schwarz, Tobias aut Wiendl, Heinz aut Budde, Thomas aut Kleinschnitz, Christoph aut Meuth, Sven G aut Enthalten in Experimental & translational stroke medicine London : BioMed Central, 2009 2(2010), 1 vom: 20. Juli (DE-627)611727404 (DE-600)2520967-X 2040-7378 nnns volume:2 year:2010 number:1 day:20 month:07 https://dx.doi.org/10.1186/2040-7378-2-14 kostenfrei 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2 2010 1 20 07 |
| language |
English |
| source |
Enthalten in Experimental & translational stroke medicine 2(2010), 1 vom: 20. Juli volume:2 year:2010 number:1 day:20 month:07 |
| sourceStr |
Enthalten in Experimental & translational stroke medicine 2(2010), 1 vom: 20. Juli volume:2 year:2010 number:1 day:20 month:07 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| topic_facet |
Cerebral Ischemia Middle Cerebral Artery Occlusion Infarct Volume Wildtype Mouse Transient Middle Cerebral Artery Occlusion |
| isfreeaccess_bool |
true |
| container_title |
Experimental & translational stroke medicine |
| authorswithroles_txt_mv |
Ehling, Petra @@aut@@ Bittner, Stefan @@aut@@ Bobak, Nicole @@aut@@ Schwarz, Tobias @@aut@@ Wiendl, Heinz @@aut@@ Budde, Thomas @@aut@@ Kleinschnitz, Christoph @@aut@@ Meuth, Sven G @@aut@@ |
| publishDateDaySort_date |
2010-07-20T00:00:00Z |
| hierarchy_top_id |
611727404 |
| id |
SPR030951070 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR030951070</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519124616.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2010 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/2040-7378-2-14</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR030951070</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)2040-7378-2-14-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Ehling, Petra</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9)</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2010</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cerebral Ischemia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Middle Cerebral Artery Occlusion</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Infarct Volume</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Wildtype Mouse</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transient Middle Cerebral Artery Occlusion</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bittner, Stefan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bobak, Nicole</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schwarz, Tobias</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wiendl, Heinz</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Budde, Thomas</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kleinschnitz, Christoph</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meuth, Sven G</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Experimental & translational stroke medicine</subfield><subfield code="d">London : BioMed Central, 2009</subfield><subfield code="g">2(2010), 1 vom: 20. Juli</subfield><subfield code="w">(DE-627)611727404</subfield><subfield code="w">(DE-600)2520967-X</subfield><subfield code="x">2040-7378</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:2</subfield><subfield code="g">year:2010</subfield><subfield code="g">number:1</subfield><subfield code="g">day:20</subfield><subfield code="g">month:07</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1186/2040-7378-2-14</subfield><subfield code="z">kostenfrei</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2005</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2055</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2111</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">2</subfield><subfield code="j">2010</subfield><subfield code="e">1</subfield><subfield code="b">20</subfield><subfield code="c">07</subfield></datafield></record></collection>
|
| author |
Ehling, Petra |
| spellingShingle |
Ehling, Petra misc Cerebral Ischemia misc Middle Cerebral Artery Occlusion misc Infarct Volume misc Wildtype Mouse misc Transient Middle Cerebral Artery Occlusion Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| authorStr |
Ehling, Petra |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)611727404 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| author_role |
aut aut aut aut aut aut aut aut |
| collection |
springer |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
2040-7378 |
| topic_title |
Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) Cerebral Ischemia (dpeaa)DE-He213 Middle Cerebral Artery Occlusion (dpeaa)DE-He213 Infarct Volume (dpeaa)DE-He213 Wildtype Mouse (dpeaa)DE-He213 Transient Middle Cerebral Artery Occlusion (dpeaa)DE-He213 |
| topic |
misc Cerebral Ischemia misc Middle Cerebral Artery Occlusion misc Infarct Volume misc Wildtype Mouse misc Transient Middle Cerebral Artery Occlusion |
| topic_unstemmed |
misc Cerebral Ischemia misc Middle Cerebral Artery Occlusion misc Infarct Volume misc Wildtype Mouse misc Transient Middle Cerebral Artery Occlusion |
| topic_browse |
misc Cerebral Ischemia misc Middle Cerebral Artery Occlusion misc Infarct Volume misc Wildtype Mouse misc Transient Middle Cerebral Artery Occlusion |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
cr |
| hierarchy_parent_title |
Experimental & translational stroke medicine |
| hierarchy_parent_id |
611727404 |
| hierarchy_top_title |
Experimental & translational stroke medicine |
| isfreeaccess_txt |
true |
| familylinks_str_mv |
(DE-627)611727404 (DE-600)2520967-X |
| title |
Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| ctrlnum |
(DE-627)SPR030951070 (SPR)2040-7378-2-14-e |
| title_full |
Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| author_sort |
Ehling, Petra |
| journal |
Experimental & translational stroke medicine |
| journalStr |
Experimental & translational stroke medicine |
| lang_code |
eng |
| isOA_bool |
true |
| recordtype |
marc |
| publishDateSort |
2010 |
| contenttype_str_mv |
txt |
| author_browse |
Ehling, Petra Bittner, Stefan Bobak, Nicole Schwarz, Tobias Wiendl, Heinz Budde, Thomas Kleinschnitz, Christoph Meuth, Sven G |
| container_volume |
2 |
| format_se |
Elektronische Aufsätze |
| author-letter |
Ehling, Petra |
| doi_str_mv |
10.1186/2040-7378-2-14 |
| title_sort |
two pore domain potassium channels in cerebral ischemia: a focus on $ k_{2p} $9.1 (task3, kcnk9) |
| title_auth |
Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| abstract |
Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia. © Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| collection_details |
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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 |
| container_issue |
1 |
| title_short |
Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9) |
| url |
https://dx.doi.org/10.1186/2040-7378-2-14 |
| remote_bool |
true |
| author2 |
Bittner, Stefan Bobak, Nicole Schwarz, Tobias Wiendl, Heinz Budde, Thomas Kleinschnitz, Christoph Meuth, Sven G |
| author2Str |
Bittner, Stefan Bobak, Nicole Schwarz, Tobias Wiendl, Heinz Budde, Thomas Kleinschnitz, Christoph Meuth, Sven G |
| ppnlink |
611727404 |
| mediatype_str_mv |
c |
| isOA_txt |
true |
| hochschulschrift_bool |
false |
| doi_str |
10.1186/2040-7378-2-14 |
| up_date |
2024-07-03T21:06:22.214Z |
| _version_ |
1803593483260264448 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR030951070</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519124616.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2010 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/2040-7378-2-14</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR030951070</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)2040-7378-2-14-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Ehling, Petra</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Two pore domain potassium channels in cerebral ischemia: a focus on $ K_{2P} $9.1 (TASK3, KCNK9)</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2010</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Ehling et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Recently, members of the two-pore domain potassium channel family ($ K_{2P} $ channels) could be shown to be involved in mechanisms contributing to neuronal damage after cerebral ischemia. $ K_{2P} $3.$ 1^{-/-} $ animals showed larger infarct volumes and a worse functional outcome following experimentally induced ischemic stroke. Here, we question the role of the closely related $ K_{2P} $ channel $ K_{2P} $9.1. Methods We combine electrophysiological recordings in brain-slice preparations of wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice with an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of $ K_{2P} $9.1 in stroke formation. Results Patch-clamp recordings reveal that currents mediated through $ K_{2P} $9.1 can be obtained in slice preparations of the dorsal lateral geniculate nucleus (dLGN) as a model of central nervous relay neurons. Current characteristics are indicative of $ K_{2P} $9.1 as they display an increase upon removal of extracellular divalent cations, an outward rectification and a reversal potential close to the potassium equilibrium potential. Lowering extracellular pH values from 7.35 to 6.0 showed comparable current reductions in neurons from wildtype and $ K_{2P} $9.$ 1^{-/-} $ mice (68.31 ± 9.80% and 69.92 ± 11.65%, respectively). These results could be translated in an in vivo model of cerebral ischemia where infarct volumes and functional outcomes showed a none significant tendency towards smaller infarct volumes in $ K_{2P} $9.$ 1^{-/-} $ animals compared to wildtype mice 24 hours after 60 min of tMCAO induction (60.50 ± 17.31 $ mm^{3} $ and 47.10 ± 19.26 $ mm^{3} $, respectively). Conclusions Together with findings from earlier studies on $ K_{2P} $2.$ 1^{-/-} $ and $ K_{2P} $3.$ 1^{-/-} $ mice, the results of the present study on $ K_{2P} $9.$ 1^{-/-} $ mice indicate a differential contribution of $ K_{2P} $ channel subtypes to the diverse and complex in vivo effects in rodent models of cerebral ischemia.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cerebral Ischemia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Middle Cerebral Artery Occlusion</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Infarct Volume</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Wildtype Mouse</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Transient Middle Cerebral Artery Occlusion</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bittner, Stefan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bobak, Nicole</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Schwarz, Tobias</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wiendl, Heinz</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Budde, Thomas</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kleinschnitz, Christoph</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meuth, Sven G</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Experimental & translational stroke medicine</subfield><subfield code="d">London : BioMed Central, 2009</subfield><subfield code="g">2(2010), 1 vom: 20. Juli</subfield><subfield code="w">(DE-627)611727404</subfield><subfield code="w">(DE-600)2520967-X</subfield><subfield code="x">2040-7378</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:2</subfield><subfield code="g">year:2010</subfield><subfield code="g">number:1</subfield><subfield code="g">day:20</subfield><subfield code="g">month:07</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.1186/2040-7378-2-14</subfield><subfield code="z">kostenfrei</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_11</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_20</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_23</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_24</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_39</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_40</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_60</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_62</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_63</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_65</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_69</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_73</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_74</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_95</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_105</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_110</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_151</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_161</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_170</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_206</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_213</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_230</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_285</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_293</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_602</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2003</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2005</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2009</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2014</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2055</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2111</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4012</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4037</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4112</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4125</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4126</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4249</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4305</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4306</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4307</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4313</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4322</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4323</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4324</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4325</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4338</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4367</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_4700</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">2</subfield><subfield code="j">2010</subfield><subfield code="e">1</subfield><subfield code="b">20</subfield><subfield code="c">07</subfield></datafield></record></collection>
|
| score |
7.4020405 |