Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation
Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbitu...
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| Autor*in: |
Naveilhan, Philippe [verfasserIn] Canals, Josep M. [verfasserIn] Arenas, Ernest [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2001 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2001 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 78(2001), 6, Seite 0 |
| Übergeordnetes Werk: |
volume:78 ; year:2001 ; number:6 ; pages:0 |
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| DOI / URN: |
10.1046/j.1471-4159.2001.00534.x |
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| 520 | |a Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. | ||
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10.1046/j.1471-4159.2001.00534.x doi (DE-627)NLEJ243141475 DE-627 ger DE-627 rakwb Naveilhan, Philippe verfasserin aut Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| anaesthesia Canals, Josep M. verfasserin aut Arenas, Ernest verfasserin aut Ernfors, Patrik oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 78(2001), 6, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:78 year:2001 number:6 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2001.00534.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 78 2001 6 0 |
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10.1046/j.1471-4159.2001.00534.x doi (DE-627)NLEJ243141475 DE-627 ger DE-627 rakwb Naveilhan, Philippe verfasserin aut Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| anaesthesia Canals, Josep M. verfasserin aut Arenas, Ernest verfasserin aut Ernfors, Patrik oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 78(2001), 6, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:78 year:2001 number:6 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2001.00534.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 78 2001 6 0 |
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10.1046/j.1471-4159.2001.00534.x doi (DE-627)NLEJ243141475 DE-627 ger DE-627 rakwb Naveilhan, Philippe verfasserin aut Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| anaesthesia Canals, Josep M. verfasserin aut Arenas, Ernest verfasserin aut Ernfors, Patrik oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 78(2001), 6, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:78 year:2001 number:6 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2001.00534.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 78 2001 6 0 |
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10.1046/j.1471-4159.2001.00534.x doi (DE-627)NLEJ243141475 DE-627 ger DE-627 rakwb Naveilhan, Philippe verfasserin aut Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| anaesthesia Canals, Josep M. verfasserin aut Arenas, Ernest verfasserin aut Ernfors, Patrik oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 78(2001), 6, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:78 year:2001 number:6 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2001.00534.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 78 2001 6 0 |
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10.1046/j.1471-4159.2001.00534.x doi (DE-627)NLEJ243141475 DE-627 ger DE-627 rakwb Naveilhan, Philippe verfasserin aut Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation Oxford, UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. 2001 Blackwell Publishing Journal Backfiles 1879-2005 |2001|||||||||| anaesthesia Canals, Josep M. verfasserin aut Arenas, Ernest verfasserin aut Ernfors, Patrik oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 78(2001), 6, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:78 year:2001 number:6 pages:0 http://dx.doi.org/10.1046/j.1471-4159.2001.00534.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 78 2001 6 0 |
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Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation anaesthesia |
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distinct roles of the y1 and y2 receptors on neuropeptide y-induced sensitization to sedation |
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Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation |
| abstract |
Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. |
| abstractGer |
Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. |
| abstract_unstemmed |
Intracranial injection of neuropeptide Y (NPY) increases the sensitivity to sodium pentobarbital and ketamin sedation and has similar properties as GABA agonists on sleep. Mice sensitive to sedation have increased levels of NPY in many brain regions and Y1−/− mice show a marked resistance to barbiturates. Here we characterized the role of the NPY Y receptors in anesthetic-induced sedation. We show that Y1 and Y2, but not Y5, receptors participate in the modulation of sedation. Administration of a Y1 agonist increased the sodium pentobarbital-induced sedation and Y1−/− mice were less sensitive to this anesthetic. However, Y2−/− mice display increased sensitivity, showing that Y2 modulates GABAergic induced sedation both pharmacologically and physiologically and has a functionally opposing role to the Y1 receptor. Analysis of Y1−/−/Y2−/− double mutant mice show that increased sensitivity by Y1 occurs independent of the Y2 receptor, while the decreased sensitivity mediated by Y2 depend on an intact Y1 receptor. In contrast to sodium pentobarbital, both Y1 and Y2 receptors increase the sensitivity in a collaborative fashion to NMDA antagonist-induced sedation. These data demonstrate the physiological and pharmacological impact of the Y1 and Y2 receptors on sedation. |
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Distinct roles of the Y1 and Y2 receptors on neuropeptide Y-induced sensitization to sedation |
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Canals, Josep M. Arenas, Ernest Ernfors, Patrik |
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