$ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons
Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic ace...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hughes, Simon [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer-Verlag 2007 |
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| Übergeordnetes Werk: |
Enthalten in: Pflügers Archiv - Berlin : Springer, 1868, 455(2007), 1 vom: 20. Apr., Seite 115-124 |
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| Übergeordnetes Werk: |
volume:455 ; year:2007 ; number:1 ; day:20 ; month:04 ; pages:115-124 |
| Links: |
|---|
| DOI / URN: |
10.1007/s00424-007-0259-6 |
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| Katalog-ID: |
SPR005608821 |
|---|
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| 100 | 1 | |a Hughes, Simon |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons |
| 264 | 1 | |c 2007 | |
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| 520 | |a Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. | ||
| 650 | 4 | |a Phosphatidylinositol-4,5-bisphosphate |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Tubby |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Phospholipase-Cδ-PH |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Muscarinic receptors |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Bradykinin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a M-current |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Sympathetic neuron |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Marsh, Stephen J. |4 aut | |
| 700 | 1 | |a Tinker, Andrew |4 aut | |
| 700 | 1 | |a Brown, David A. |4 aut | |
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10.1007/s00424-007-0259-6 doi (DE-627)SPR005608821 (SPR)s00424-007-0259-6-e DE-627 ger DE-627 rakwb eng Hughes, Simon verfasserin aut $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2007 Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 Marsh, Stephen J. aut Tinker, Andrew aut Brown, David A. aut Enthalten in Pflügers Archiv Berlin : Springer, 1868 455(2007), 1 vom: 20. Apr., Seite 115-124 (DE-627)25463897X (DE-600)1463014-X 1432-2013 nnns volume:455 year:2007 number:1 day:20 month:04 pages:115-124 https://dx.doi.org/10.1007/s00424-007-0259-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 455 2007 1 20 04 115-124 |
| spelling |
10.1007/s00424-007-0259-6 doi (DE-627)SPR005608821 (SPR)s00424-007-0259-6-e DE-627 ger DE-627 rakwb eng Hughes, Simon verfasserin aut $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2007 Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 Marsh, Stephen J. aut Tinker, Andrew aut Brown, David A. aut Enthalten in Pflügers Archiv Berlin : Springer, 1868 455(2007), 1 vom: 20. Apr., Seite 115-124 (DE-627)25463897X (DE-600)1463014-X 1432-2013 nnns volume:455 year:2007 number:1 day:20 month:04 pages:115-124 https://dx.doi.org/10.1007/s00424-007-0259-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 455 2007 1 20 04 115-124 |
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10.1007/s00424-007-0259-6 doi (DE-627)SPR005608821 (SPR)s00424-007-0259-6-e DE-627 ger DE-627 rakwb eng Hughes, Simon verfasserin aut $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2007 Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 Marsh, Stephen J. aut Tinker, Andrew aut Brown, David A. aut Enthalten in Pflügers Archiv Berlin : Springer, 1868 455(2007), 1 vom: 20. Apr., Seite 115-124 (DE-627)25463897X (DE-600)1463014-X 1432-2013 nnns volume:455 year:2007 number:1 day:20 month:04 pages:115-124 https://dx.doi.org/10.1007/s00424-007-0259-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 455 2007 1 20 04 115-124 |
| allfieldsGer |
10.1007/s00424-007-0259-6 doi (DE-627)SPR005608821 (SPR)s00424-007-0259-6-e DE-627 ger DE-627 rakwb eng Hughes, Simon verfasserin aut $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2007 Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 Marsh, Stephen J. aut Tinker, Andrew aut Brown, David A. aut Enthalten in Pflügers Archiv Berlin : Springer, 1868 455(2007), 1 vom: 20. Apr., Seite 115-124 (DE-627)25463897X (DE-600)1463014-X 1432-2013 nnns volume:455 year:2007 number:1 day:20 month:04 pages:115-124 https://dx.doi.org/10.1007/s00424-007-0259-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 455 2007 1 20 04 115-124 |
| allfieldsSound |
10.1007/s00424-007-0259-6 doi (DE-627)SPR005608821 (SPR)s00424-007-0259-6-e DE-627 ger DE-627 rakwb eng Hughes, Simon verfasserin aut $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag 2007 Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 Marsh, Stephen J. aut Tinker, Andrew aut Brown, David A. aut Enthalten in Pflügers Archiv Berlin : Springer, 1868 455(2007), 1 vom: 20. Apr., Seite 115-124 (DE-627)25463897X (DE-600)1463014-X 1432-2013 nnns volume:455 year:2007 number:1 day:20 month:04 pages:115-124 https://dx.doi.org/10.1007/s00424-007-0259-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 455 2007 1 20 04 115-124 |
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English |
| source |
Enthalten in Pflügers Archiv 455(2007), 1 vom: 20. Apr., Seite 115-124 volume:455 year:2007 number:1 day:20 month:04 pages:115-124 |
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Enthalten in Pflügers Archiv 455(2007), 1 vom: 20. Apr., Seite 115-124 volume:455 year:2007 number:1 day:20 month:04 pages:115-124 |
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Article |
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findex.gbv.de |
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Phosphatidylinositol-4,5-bisphosphate Tubby Phospholipase-Cδ-PH Muscarinic receptors Bradykinin M-current Sympathetic neuron |
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Hughes, Simon @@aut@@ Marsh, Stephen J. @@aut@@ Tinker, Andrew @@aut@@ Brown, David A. @@aut@@ |
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2007-04-20T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR005608821</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230507182545.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201002s2007 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00424-007-0259-6</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR005608821</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00424-007-0259-6-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">Hughes, Simon</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">$ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2007</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">© Springer-Verlag 2007</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. 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Hughes, Simon |
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Hughes, Simon misc Phosphatidylinositol-4,5-bisphosphate misc Tubby misc Phospholipase-Cδ-PH misc Muscarinic receptors misc Bradykinin misc M-current misc Sympathetic neuron $ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons |
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$ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons Phosphatidylinositol-4,5-bisphosphate (dpeaa)DE-He213 Tubby (dpeaa)DE-He213 Phospholipase-Cδ-PH (dpeaa)DE-He213 Muscarinic receptors (dpeaa)DE-He213 Bradykinin (dpeaa)DE-He213 M-current (dpeaa)DE-He213 Sympathetic neuron (dpeaa)DE-He213 |
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115 |
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Hughes, Simon Marsh, Stephen J. Tinker, Andrew Brown, David A. |
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Elektronische Aufsätze |
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Hughes, Simon |
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10.1007/s00424-007-0259-6 |
| title_sort |
$ pip_{2} $-dependent inhibition of m-type (kv7.2/7.3) potassium channels: direct on-line assessment of $ pip_{2} $ depletion by gq-coupled receptors in single living neurons |
| title_auth |
$ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons |
| abstract |
Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. © Springer-Verlag 2007 |
| abstractGer |
Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. © Springer-Verlag 2007 |
| abstract_unstemmed |
Abstract The open state of M(Kv7.2/7.3) potassium channels is maintained by membrane phosphatidylinositol-4,5-bisphosphate (PI(4,5)$ P_{2} $). They can be closed on stimulating receptors that induce PI(4,5)$ P_{2} $ hydrolysis. In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)$ P_{2} $, whereas closure by bradykinin $ B_{2} $-receptors (B2-BKRs) appears to result from formation of $ IP_{3} $ and release of $ Ca^{2+} $, implying that BKR stimulation does not deplete PI(4,5)$ P_{2} $. We have used a fluorescently tagged PI(4,5)$ P_{2} $-binding construct, the C-domain of the protein tubby, mutated to increase sensitivity to PI(4,5)$ P_{2} $ changes (tubby-R332H-cYFP), to provide an on-line read-out of PI(4,5)$ P_{2} $ changes in single living sympathetic neurons after receptor stimulation. We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation. However, translocation by BK was increased to equal that produced by oxo-M when synthesis of PI(4,5)$ P_{2} $ was inhibited by wortmannin. Further, wortmannin ‘rescued’ M-current inhibition by BK after $ Ca^{2+} $-dependent inhibition was reduced by thapsigargin. These results provide the first direct support for the view that BK accelerates PI(4,5)$ P_{2} $ synthesis in these neurons, and show that the mechanism of BKR-induced inhibition can be switched from $ Ca^{2+} $ dependent to PI(4,5)$ P_{2} $ dependent when PI(4,5)$ P_{2} $ synthesis is inhibited. © Springer-Verlag 2007 |
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$ PIP_{2} $-dependent inhibition of M-type (Kv7.2/7.3) potassium channels: direct on-line assessment of $ PIP_{2} $ depletion by Gq-coupled receptors in single living neurons |
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| score |
7.399721 |