Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective
Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreas...
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| Autor*in: |
Woodward, John J. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science, Ltd ; 2002 |
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| Umfang: |
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), 4, Seite 0 |
| Übergeordnetes Werk: |
volume:80 ; year:2002 ; number:4 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.0022-3042.2001.00736.x |
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| 520 | |a Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. | ||
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10.1046/j.0022-3042.2001.00736.x doi (DE-627)NLEJ243139268 DE-627 ger DE-627 rakwb Woodward, John J. verfasserin aut Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| electrophysiology In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 4 0 |
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10.1046/j.0022-3042.2001.00736.x doi (DE-627)NLEJ243139268 DE-627 ger DE-627 rakwb Woodward, John J. verfasserin aut Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| electrophysiology In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 4 0 |
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10.1046/j.0022-3042.2001.00736.x doi (DE-627)NLEJ243139268 DE-627 ger DE-627 rakwb Woodward, John J. verfasserin aut Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| electrophysiology In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 4 0 |
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10.1046/j.0022-3042.2001.00736.x doi (DE-627)NLEJ243139268 DE-627 ger DE-627 rakwb Woodward, John J. verfasserin aut Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| electrophysiology In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 4 0 |
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10.1046/j.0022-3042.2001.00736.x doi (DE-627)NLEJ243139268 DE-627 ger DE-627 rakwb Woodward, John J. verfasserin aut Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective Oxford, UK Blackwell Science, Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| electrophysiology In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 80(2002), 4, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:80 year:2002 number:4 pages:0 http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 80 2002 4 0 |
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prostacyclin-induced rundown of n-methyl-d-aspartate receptor currents in hek293 cells is protein kinase a-dependent and nr2 subunit-selective |
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Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective |
| abstract |
Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. |
| abstractGer |
Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. |
| abstract_unstemmed |
Previous studies in neurons have demonstrated a rapid decrease in NMDA receptor currents following tyrosine kinase inhibition or exposure to platelet-derived growth factor (PDGF). Inhibitors of protein kinase A␣(PKA) block the PDGF-induced rundown suggesting a multistep pathway that leads to decreased amplitudes of NMDA-activated currents. In this study, HEK293 cells expressing different NMDA receptor subunits were used to study the effects of prostacyclin receptor-mediated PKA activation on the magnitude of glutamate-activated currents. The prostacyclin agonist iloprost induced a rapid and time-dependent depression of otherwise stable glutamate-activated currents in cells expressing NR1–2a/2A or NR1–2a/2D receptors but not NR1–2a/2B or NR1–2a/2C receptors. This rundown was prevented by treatment of cells with the PKA inhibitor H89. The iloprost effect persisted in cells coexpressing NR1–2a/2A receptors and either wild-type or mutant Src kinase (SrcS17A). Co-expression of PSD-95 with NR1–2a/2A receptors reduced but did not eliminate the extent of rundown. Iloprost also produced current rundown in cells expressing NR1–2a and a C-terminal truncated NR2A subunit (NR2A1050stop) but not in those transfected with an NR2A tyrosine mutant (Y842F). The iloprost-induced rundown of wild-type NR1–2a/2A receptors was prevented by prior exposure of cells to hypertonic sucrose. These results suggest that PKA influences the functional activity of NMDA receptors in an NR2 subunit-selective fashion. |
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| title_short |
Prostacyclin-induced rundown of N-methyl-d-aspartate receptor currents in HEK293 cells is protein kinase A-dependent and NR2 subunit-selective |
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http://dx.doi.org/10.1046/j.0022-3042.2001.00736.x |
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