Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones

Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienc...
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Autor*in:	Gruss, Marco Ettorre, Giovanni Jana Stehr, Annette Henrich, Michael Hempelmann, Gunter Scholz, Andreas

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2006

Umfang:	Online-Ressource (PDF-Datei: 14 S., 1,35 MB)
Beschreibung:	Systemvoraussetzungen: Acrobat reader.

Übergeordnetes Werk:	In: Biomedical engineering online - London : BioMed Central, 2002, 2(2006), 12, Seite 1-14
Übergeordnetes Werk:	volume:2 ; year:2006 ; number:12 ; pages:1-14

Links:	Volltext Volltext

Katalog-ID:	525569804

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245	1	0	\|a Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones \|c Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz
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520			\|a Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia
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allfields	(DE-627)525569804 (DE-599)GBV525569804 DE-627 ger DE-627 rakwb eng 610 617.96 44.90 bkl Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz 2006 Online-Ressource (PDF-Datei: 14 S., 1,35 MB) Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia Systemvoraussetzungen: Acrobat reader. Gruss, Marco oth Ettorre, Giovanni oth Jana Stehr, Annette oth Henrich, Michael oth Hempelmann, Gunter oth Scholz, Andreas oth In Biomedical engineering online London : BioMed Central, 2002 2(2006), 12, Seite 1-14 Online-Ressource (DE-627)35210547X (DE-600)2084374-4 (DE-576)107015161 1475-925X nnns volume:2 year:2006 number:12 pages:1-14 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf Verlag Volltext http://dx.doi.org/10.1186/1744-8069-2-12 Resolving-System Volltext GBV_USEFLAG_U GBV_ILN_40 ISIL_DE-7 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 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_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_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2119 GBV_ILN_2190 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.90 Neurologie (DE-627)106409980 AR 2 2006 12 1-14 40 01 0007 815471505 goescholar ksn 22-01-08 40 01 0007 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf 40 01 0007 http://dx.doi.org/10.1186/1744-8069-2-12 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin 40 00 DE-7 00 (DE-627)619876255 MED 531 Neuroanatomie, Neurophysiologie, Neuropathologie 40 01 0007 goescholar 40 01 0007 univdok 40 01 0007 2008-01 9
spelling	(DE-627)525569804 (DE-599)GBV525569804 DE-627 ger DE-627 rakwb eng 610 617.96 44.90 bkl Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz 2006 Online-Ressource (PDF-Datei: 14 S., 1,35 MB) Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia Systemvoraussetzungen: Acrobat reader. Gruss, Marco oth Ettorre, Giovanni oth Jana Stehr, Annette oth Henrich, Michael oth Hempelmann, Gunter oth Scholz, Andreas oth In Biomedical engineering online London : BioMed Central, 2002 2(2006), 12, Seite 1-14 Online-Ressource (DE-627)35210547X (DE-600)2084374-4 (DE-576)107015161 1475-925X nnns volume:2 year:2006 number:12 pages:1-14 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf Verlag Volltext http://dx.doi.org/10.1186/1744-8069-2-12 Resolving-System Volltext GBV_USEFLAG_U GBV_ILN_40 ISIL_DE-7 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 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_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_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2119 GBV_ILN_2190 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.90 Neurologie (DE-627)106409980 AR 2 2006 12 1-14 40 01 0007 815471505 goescholar ksn 22-01-08 40 01 0007 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf 40 01 0007 http://dx.doi.org/10.1186/1744-8069-2-12 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin 40 00 DE-7 00 (DE-627)619876255 MED 531 Neuroanatomie, Neurophysiologie, Neuropathologie 40 01 0007 goescholar 40 01 0007 univdok 40 01 0007 2008-01 9
allfields_unstemmed	(DE-627)525569804 (DE-599)GBV525569804 DE-627 ger DE-627 rakwb eng 610 617.96 44.90 bkl Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz 2006 Online-Ressource (PDF-Datei: 14 S., 1,35 MB) Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia Systemvoraussetzungen: Acrobat reader. Gruss, Marco oth Ettorre, Giovanni oth Jana Stehr, Annette oth Henrich, Michael oth Hempelmann, Gunter oth Scholz, Andreas oth In Biomedical engineering online London : BioMed Central, 2002 2(2006), 12, Seite 1-14 Online-Ressource (DE-627)35210547X (DE-600)2084374-4 (DE-576)107015161 1475-925X nnns volume:2 year:2006 number:12 pages:1-14 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf Verlag Volltext http://dx.doi.org/10.1186/1744-8069-2-12 Resolving-System Volltext GBV_USEFLAG_U GBV_ILN_40 ISIL_DE-7 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 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_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_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2119 GBV_ILN_2190 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.90 Neurologie (DE-627)106409980 AR 2 2006 12 1-14 40 01 0007 815471505 goescholar ksn 22-01-08 40 01 0007 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf 40 01 0007 http://dx.doi.org/10.1186/1744-8069-2-12 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin 40 00 DE-7 00 (DE-627)619876255 MED 531 Neuroanatomie, Neurophysiologie, Neuropathologie 40 01 0007 goescholar 40 01 0007 univdok 40 01 0007 2008-01 9
allfieldsGer	(DE-627)525569804 (DE-599)GBV525569804 DE-627 ger DE-627 rakwb eng 610 617.96 44.90 bkl Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz 2006 Online-Ressource (PDF-Datei: 14 S., 1,35 MB) Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia Systemvoraussetzungen: Acrobat reader. Gruss, Marco oth Ettorre, Giovanni oth Jana Stehr, Annette oth Henrich, Michael oth Hempelmann, Gunter oth Scholz, Andreas oth In Biomedical engineering online London : BioMed Central, 2002 2(2006), 12, Seite 1-14 Online-Ressource (DE-627)35210547X (DE-600)2084374-4 (DE-576)107015161 1475-925X nnns volume:2 year:2006 number:12 pages:1-14 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf Verlag Volltext http://dx.doi.org/10.1186/1744-8069-2-12 Resolving-System Volltext GBV_USEFLAG_U GBV_ILN_40 ISIL_DE-7 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 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_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_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2119 GBV_ILN_2190 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.90 Neurologie (DE-627)106409980 AR 2 2006 12 1-14 40 01 0007 815471505 goescholar ksn 22-01-08 40 01 0007 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf 40 01 0007 http://dx.doi.org/10.1186/1744-8069-2-12 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin 40 00 DE-7 00 (DE-627)619876255 MED 531 Neuroanatomie, Neurophysiologie, Neuropathologie 40 01 0007 goescholar 40 01 0007 univdok 40 01 0007 2008-01 9
allfieldsSound	(DE-627)525569804 (DE-599)GBV525569804 DE-627 ger DE-627 rakwb eng 610 617.96 44.90 bkl Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz 2006 Online-Ressource (PDF-Datei: 14 S., 1,35 MB) Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia Systemvoraussetzungen: Acrobat reader. Gruss, Marco oth Ettorre, Giovanni oth Jana Stehr, Annette oth Henrich, Michael oth Hempelmann, Gunter oth Scholz, Andreas oth In Biomedical engineering online London : BioMed Central, 2002 2(2006), 12, Seite 1-14 Online-Ressource (DE-627)35210547X (DE-600)2084374-4 (DE-576)107015161 1475-925X nnns volume:2 year:2006 number:12 pages:1-14 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf Verlag Volltext http://dx.doi.org/10.1186/1744-8069-2-12 Resolving-System Volltext GBV_USEFLAG_U GBV_ILN_40 ISIL_DE-7 SYSFLAG_1 GBV_KXP SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 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_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_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2119 GBV_ILN_2190 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_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.90 Neurologie (DE-627)106409980 AR 2 2006 12 1-14 40 01 0007 815471505 goescholar ksn 22-01-08 40 01 0007 http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf 40 01 0007 http://dx.doi.org/10.1186/1744-8069-2-12 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin 40 00 DE-7 00 (DE-627)619876255 MED 531 Neuroanatomie, Neurophysiologie, Neuropathologie 40 01 0007 goescholar 40 01 0007 univdok 40 01 0007 2008-01 9
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authorswithroles_txt_mv	Gruss, Marco @@oth@@ Ettorre, Giovanni @@oth@@ Jana Stehr, Annette @@oth@@ Henrich, Michael @@oth@@ Hempelmann, Gunter @@oth@@ Scholz, Andreas @@oth@@
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topic_title	610 617.96 44.90 bkl 40 01 0007 90 (DE-627)525004262 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz
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spellingShingle	ddc 610 ddc 617.96 bkl 44.90 40 Zentrum 18 Anaesthesiologie, Rettungs- und Intensivmedizin Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones
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title	Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones
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title_full	Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz
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title_sort	moderate hypoxia influences excitability and blocks dendrotoxin sensitive k+ currents in rat primary sensory neurones
title_auth	Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones
abstract	Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia
abstractGer	Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia
abstract_unstemmed	Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. Altogether these results, might explain the functional impairment of peripheral neurones under moderate hypoxia
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title_short	Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones
url	http://webdoc.sub.gwdg.de/pub/med/2007/biomed/2006-stehr.pdf http://dx.doi.org/10.1186/1744-8069-2-12
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">525569804</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20240130054359.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070308s2006 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)525569804</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBV525569804</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="082" ind1="0" ind2="4"><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">617.96</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones</subfield><subfield code="c">Marco Gruss, Giovanni Ettorre, Annette Jana Stehr, Michael Henrich, Gunter Hempelmann and Andreas Scholz</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2006</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource (PDF-Datei: 14 S., 1,35 MB)</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="520" ind1=" " ind2=" "><subfield code="a">Abstract: Hypoxia alters neuronal function and can lead to neuronal injury or death especially in the central nervous system. But little is known about the effects of hypoxia in neurones of the peripheral nervous system (PNS), which survive longer hypoxic periods. Additionally, people have experienced unpleasant sensations during ischemia which are dedicated to changes in conduction properties or changes in excitability in the PNS. However, the underlying ionic conductances in dorsal root ganglion (DRG) neurones have not been investigated in detail. Therefore we investigated the influence of moderate hypoxia (27.0 ± 1.5 mmHg) on action potentials, excitability and ionic conductances of small neurones in a slice preparation of DRGs of young rats. The neurones responded within a few minutes non-uniformly to moderate hypoxia: changes of excitability could be assigned to decreased outward currents in most of the neurones (77%) whereas a smaller group (23%) displayed increased outward currents in Ringer solution. We were able to attribute most of the reduction in outward-current to a voltage-gated K+ current which activated at potentials positive to -50 mV and was sensitive to 50 nM a-dendrotoxin (DTX). Other toxins that inhibit subtypes of voltage gated K+ channels, such as margatoxin (MgTX), dendrotoxin-K (DTX-K), r-tityustoxin Ka (TsTX-K) and r-agitoxin (AgTX-2) failed to prevent the hypoxia induced reduction. Therefore we could not assign the hypoxia sensitive K+ current to one homomeric KV channel type in sensory neurones. Functionally this K+ current blockade might underlie the increased action potential (AP) duration in these neurones. 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Moderate hypoxia influences excitability and blocks dendrotoxin sensitive K+ currents in rat primary sensory neurones

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