Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement
Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by...
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| Autor*in: |
Kendall, David A. [verfasserIn] Nahorski, Stefan R. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1984 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 42(1984), 5, Seite 0 |
| Übergeordnetes Werk: |
volume:42 ; year:1984 ; number:5 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1111/j.1471-4159.1984.tb02799.x |
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| 520 | |a Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. | ||
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10.1111/j.1471-4159.1984.tb02799.x doi (DE-627)NLEJ240305272 DE-627 ger DE-627 rakwb Kendall, David A. verfasserin aut Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement Oxford, UK Blackwell Publishing Ltd 1984 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Inositol phospholipids Nahorski, Stefan R. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 42(1984), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:42 year:1984 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1984.tb02799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 42 1984 5 0 |
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10.1111/j.1471-4159.1984.tb02799.x doi (DE-627)NLEJ240305272 DE-627 ger DE-627 rakwb Kendall, David A. verfasserin aut Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement Oxford, UK Blackwell Publishing Ltd 1984 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Inositol phospholipids Nahorski, Stefan R. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 42(1984), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:42 year:1984 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1984.tb02799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 42 1984 5 0 |
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10.1111/j.1471-4159.1984.tb02799.x doi (DE-627)NLEJ240305272 DE-627 ger DE-627 rakwb Kendall, David A. verfasserin aut Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement Oxford, UK Blackwell Publishing Ltd 1984 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Inositol phospholipids Nahorski, Stefan R. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 42(1984), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:42 year:1984 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1984.tb02799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 42 1984 5 0 |
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10.1111/j.1471-4159.1984.tb02799.x doi (DE-627)NLEJ240305272 DE-627 ger DE-627 rakwb Kendall, David A. verfasserin aut Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement Oxford, UK Blackwell Publishing Ltd 1984 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Inositol phospholipids Nahorski, Stefan R. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 42(1984), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:42 year:1984 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1984.tb02799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 42 1984 5 0 |
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10.1111/j.1471-4159.1984.tb02799.x doi (DE-627)NLEJ240305272 DE-627 ger DE-627 rakwb Kendall, David A. verfasserin aut Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement Oxford, UK Blackwell Publishing Ltd 1984 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Inositol phospholipids Nahorski, Stefan R. verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 42(1984), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:42 year:1984 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.1984.tb02799.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 42 1984 5 0 |
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inositol phospholipid hydrolysis in rat cerebral cortical slices: ii. calcium requirement |
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Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement |
| abstract |
Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. |
| abstractGer |
Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. |
| abstract_unstemmed |
Abstract: The calcium requirement for agonist-dependent breakdown of phosphatidylinositol and polyphos-phoinositides has been examined in rat cerebral cortex. The omission of added Ca2+ from the incubation medium abolished [3H]inositol phosphate accumulation from prelabelled phospholipid induced by histamine, reduced that due to noradrenaline and 5-hydroxytryptamine, but did not affect carbachol-stimulated breakdown. EC50 values for agonists were unaltered in the absence of Ca2+. Removal of Ca2+ by preincubation with EGTA (0.5 mM) abolished all responses, but complete restoration was achieved by replacement of Ca2+. The EC50for Ca2+ for histamine-stimulated [3H]inositol phosphate accumulation was 80 μM. Noradrenaline-stimulated breakdown was antagonised by manganese (IC50 1.7 mM), but not by the calcium channel blockers nitrendipine or nimodipine (30 μM). The calcium ionophore A23187 stimulated phosphatidylinositol/polyphosphoinositide hydrolysis with an EC50 of 2 μM, and this response was blocked by EGTA. Omission of Ca2+ or preincubation with EGTA or Mn2+ (EC50= 230 μM) greatly enhanced the incorporation of [3H]inositol into phospholipids. The IC50for Ca2+ in inhibiting incorporation was 25 μM. The results show that different receptors mediating phosphatidylinositol/ polyphosphoinositide breakdown in rat cortex have quantitatively different Ca2+ requirements, and it is suggested that rigid opinions regarding phosphatidylinositol/ polyphosphoinositide breakdown as either cause or effect of calcium mobilisation in rat cortex are inappropriate. |
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Inositol Phospholipid Hydrolysis in Rat Cerebral Cortical Slices: II. Calcium Requirement |
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