A homeostatic mechanism counteracting K+-evoked choline release in adult brain
Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingl...
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| Autor*in: |
Klein, Jochen [verfasserIn] Weichel, Oksana [verfasserIn] Ruhr, Judith [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science, Ltd ; 2002 |
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Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 80(2002), 5, Seite 0 |
| Übergeordnetes Werk: |
volume:80 ; year:2002 ; number:5 ; pages:0 |
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| DOI / URN: |
10.1046/j.0022-3042.2001.00754.x |
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| 520 | |a Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. | ||
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10.1046/j.0022-3042.2001.00754.x doi (DE-627)NLEJ243138954 DE-627 ger DE-627 rakwb Klein, Jochen verfasserin aut A homeostatic mechanism counteracting K+-evoked choline release in adult brain Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Weichel, Oksana verfasserin aut Ruhr, Judith verfasserin aut Dvorak, Claudia oth Löffelholz, Konrad oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:5 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 5 0 |
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10.1046/j.0022-3042.2001.00754.x doi (DE-627)NLEJ243138954 DE-627 ger DE-627 rakwb Klein, Jochen verfasserin aut A homeostatic mechanism counteracting K+-evoked choline release in adult brain Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Weichel, Oksana verfasserin aut Ruhr, Judith verfasserin aut Dvorak, Claudia oth Löffelholz, Konrad oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:5 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 5 0 |
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10.1046/j.0022-3042.2001.00754.x doi (DE-627)NLEJ243138954 DE-627 ger DE-627 rakwb Klein, Jochen verfasserin aut A homeostatic mechanism counteracting K+-evoked choline release in adult brain Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Weichel, Oksana verfasserin aut Ruhr, Judith verfasserin aut Dvorak, Claudia oth Löffelholz, Konrad oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:5 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 5 0 |
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10.1046/j.0022-3042.2001.00754.x doi (DE-627)NLEJ243138954 DE-627 ger DE-627 rakwb Klein, Jochen verfasserin aut A homeostatic mechanism counteracting K+-evoked choline release in adult brain Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Weichel, Oksana verfasserin aut Ruhr, Judith verfasserin aut Dvorak, Claudia oth Löffelholz, Konrad oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:5 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 5 0 |
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10.1046/j.0022-3042.2001.00754.x doi (DE-627)NLEJ243138954 DE-627 ger DE-627 rakwb Klein, Jochen verfasserin aut A homeostatic mechanism counteracting K+-evoked choline release in adult brain Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Weichel, Oksana verfasserin aut Ruhr, Judith verfasserin aut Dvorak, Claudia oth Löffelholz, Konrad oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:5 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00754.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 5 0 |
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A homeostatic mechanism counteracting K+-evoked choline release in adult brain |
| abstract |
Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. |
| abstractGer |
Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. |
| abstract_unstemmed |
Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+-evoked Ch release was Ca2+-independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+-induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1-week-old rats, high K+ as well as 4-aminopyridine evoked a marked Ch efflux in a concentration-dependent fashion. This phenomenon faded within 1 week. Hemicholinium-3 (HC-3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+-independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells. |
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A homeostatic mechanism counteracting K+-evoked choline release in adult brain |
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Weichel, Oksana Ruhr, Judith Dvorak, Claudia Löffelholz, Konrad |
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10.1046/j.0022-3042.2001.00754.x |
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