Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons
Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical...
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Gespeichert in:
| Autor*in: |
Parkinson, Fiona E. [verfasserIn] Xiong, Wei [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2004 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2004 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 88(2004), 5, Seite 0 |
| Übergeordnetes Werk: |
volume:88 ; year:2004 ; number:5 ; pages:0 |
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| DOI / URN: |
10.1046/j.1471-4159.2003.02266.x |
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| 520 | |a Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. | ||
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10.1046/j.1471-4159.2003.02266.x doi (DE-627)NLEJ243124066 DE-627 ger DE-627 rakwb Parkinson, Fiona E. verfasserin aut Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| adenosine 5′-monophosphate deaminase Xiong, Wei verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:5 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02266.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 5 0 |
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10.1046/j.1471-4159.2003.02266.x doi (DE-627)NLEJ243124066 DE-627 ger DE-627 rakwb Parkinson, Fiona E. verfasserin aut Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| adenosine 5′-monophosphate deaminase Xiong, Wei verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:5 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02266.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 5 0 |
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10.1046/j.1471-4159.2003.02266.x doi (DE-627)NLEJ243124066 DE-627 ger DE-627 rakwb Parkinson, Fiona E. verfasserin aut Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| adenosine 5′-monophosphate deaminase Xiong, Wei verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:5 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02266.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 5 0 |
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10.1046/j.1471-4159.2003.02266.x doi (DE-627)NLEJ243124066 DE-627 ger DE-627 rakwb Parkinson, Fiona E. verfasserin aut Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| adenosine 5′-monophosphate deaminase Xiong, Wei verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:5 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02266.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 5 0 |
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10.1046/j.1471-4159.2003.02266.x doi (DE-627)NLEJ243124066 DE-627 ger DE-627 rakwb Parkinson, Fiona E. verfasserin aut Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons Oxford, UK Blackwell Science Ltd 2004 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. 2004 Blackwell Publishing Journal Backfiles 1879-2005 |2004|||||||||| adenosine 5′-monophosphate deaminase Xiong, Wei verfasserin aut In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 88(2004), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:88 year:2004 number:5 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2003.02266.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 88 2004 5 0 |
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Stimulus- and cell-type-specific release of purines in cultured rat forebrain astrocytes and neurons |
| abstract |
Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. |
| abstractGer |
Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. |
| abstract_unstemmed |
Adenosine is formed during conditions that deplete ATP, such as ischemia. Adenosine deaminase converts adenosine into inosine, and both adenosine and inosine can be beneficial for postischemic recovery. This study investigated adenosine and inosine release from astrocytes and neurons during chemical hypoxia or oxygen–glucose deprivation. In both cell types, 2-deoxyglucose was the most effective stimulus for depleting cellular ATP and for evoking inosine release; in contrast, oxygen–glucose deprivation evoked the greatest adenosine release. α,β-Methylene ADP, an inhibitor of ecto-5′nucleotidase, significantly reduced adenosine release from astrocytes but not neurons. Dipyridamole, an inhibitor of equilibrative nucleoside transporters, inhibited both adenosine and inosine release from neurons. Erythro-9-(2-hydroxy-3-nonyl)adenine, an inhibitor of adenosine deaminase, reduced neuronal inosine release evoked by oxygen–glucose deprivation but not by 2-deoxyglucose treatment. These data indicate that (1) astrocytes release adenine nucleotides that are hydrolyzed extracellularly to adenosine, whereas neurons release adenosine per se, (2) inosine is formed intracellularly and released via nucleoside transporters, and (3) inosine is formed by an adenosine deaminase-dependent pathway during oxygen–glucose deprivation but not during 2-deoxyglucose treatment. In summary, the metabolic pathways for adenosine formation and release were cell-type dependent whereas the pathways for inosine formation were stimulus dependent. |
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