Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress
Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Vinkers, Christiaan H. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s) 2009 |
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| Übergeordnetes Werk: |
Enthalten in: Psychopharmacology - Berlin : Springer, 1959, 204(2009), 2 vom: 24. Jan., Seite 299-311 |
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| Übergeordnetes Werk: |
volume:204 ; year:2009 ; number:2 ; day:24 ; month:01 ; pages:299-311 |
| Links: |
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| DOI / URN: |
10.1007/s00213-009-1460-4 |
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SPR00201081X |
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| 024 | 7 | |a 10.1007/s00213-009-1460-4 |2 doi | |
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| 100 | 1 | |a Vinkers, Christiaan H. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
| 264 | 1 | |c 2009 | |
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| 520 | |a Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. | ||
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| 650 | 4 | |a Stress-induced hyperthermia |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Body temperature |7 (dpeaa)DE-He213 | |
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| 700 | 1 | |a Klanker, Marianne |4 aut | |
| 700 | 1 | |a Groenink, Lucianne |4 aut | |
| 700 | 1 | |a Korte, S. Mechiel |4 aut | |
| 700 | 1 | |a Cook, James M. |4 aut | |
| 700 | 1 | |a Van Linn, Michael L. |4 aut | |
| 700 | 1 | |a Hopkins, Seth C. |4 aut | |
| 700 | 1 | |a Olivier, Berend |4 aut | |
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10.1007/s00213-009-1460-4 doi (DE-627)SPR00201081X (SPR)s00213-009-1460-4-e DE-627 ger DE-627 rakwb eng Vinkers, Christiaan H. verfasserin aut Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2009 Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 Klanker, Marianne aut Groenink, Lucianne aut Korte, S. Mechiel aut Cook, James M. aut Van Linn, Michael L. aut Hopkins, Seth C. aut Olivier, Berend aut Enthalten in Psychopharmacology Berlin : Springer, 1959 204(2009), 2 vom: 24. Jan., Seite 299-311 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:204 year:2009 number:2 day:24 month:01 pages:299-311 https://dx.doi.org/10.1007/s00213-009-1460-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 204 2009 2 24 01 299-311 |
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10.1007/s00213-009-1460-4 doi (DE-627)SPR00201081X (SPR)s00213-009-1460-4-e DE-627 ger DE-627 rakwb eng Vinkers, Christiaan H. verfasserin aut Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2009 Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 Klanker, Marianne aut Groenink, Lucianne aut Korte, S. Mechiel aut Cook, James M. aut Van Linn, Michael L. aut Hopkins, Seth C. aut Olivier, Berend aut Enthalten in Psychopharmacology Berlin : Springer, 1959 204(2009), 2 vom: 24. Jan., Seite 299-311 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:204 year:2009 number:2 day:24 month:01 pages:299-311 https://dx.doi.org/10.1007/s00213-009-1460-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 204 2009 2 24 01 299-311 |
| allfields_unstemmed |
10.1007/s00213-009-1460-4 doi (DE-627)SPR00201081X (SPR)s00213-009-1460-4-e DE-627 ger DE-627 rakwb eng Vinkers, Christiaan H. verfasserin aut Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2009 Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 Klanker, Marianne aut Groenink, Lucianne aut Korte, S. Mechiel aut Cook, James M. aut Van Linn, Michael L. aut Hopkins, Seth C. aut Olivier, Berend aut Enthalten in Psychopharmacology Berlin : Springer, 1959 204(2009), 2 vom: 24. Jan., Seite 299-311 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:204 year:2009 number:2 day:24 month:01 pages:299-311 https://dx.doi.org/10.1007/s00213-009-1460-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 204 2009 2 24 01 299-311 |
| allfieldsGer |
10.1007/s00213-009-1460-4 doi (DE-627)SPR00201081X (SPR)s00213-009-1460-4-e DE-627 ger DE-627 rakwb eng Vinkers, Christiaan H. verfasserin aut Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2009 Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 Klanker, Marianne aut Groenink, Lucianne aut Korte, S. Mechiel aut Cook, James M. aut Van Linn, Michael L. aut Hopkins, Seth C. aut Olivier, Berend aut Enthalten in Psychopharmacology Berlin : Springer, 1959 204(2009), 2 vom: 24. Jan., Seite 299-311 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:204 year:2009 number:2 day:24 month:01 pages:299-311 https://dx.doi.org/10.1007/s00213-009-1460-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 204 2009 2 24 01 299-311 |
| allfieldsSound |
10.1007/s00213-009-1460-4 doi (DE-627)SPR00201081X (SPR)s00213-009-1460-4-e DE-627 ger DE-627 rakwb eng Vinkers, Christiaan H. verfasserin aut Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2009 Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 Klanker, Marianne aut Groenink, Lucianne aut Korte, S. Mechiel aut Cook, James M. aut Van Linn, Michael L. aut Hopkins, Seth C. aut Olivier, Berend aut Enthalten in Psychopharmacology Berlin : Springer, 1959 204(2009), 2 vom: 24. Jan., Seite 299-311 (DE-627)341342254 (DE-600)2066933-1 1432-2072 nnns volume:204 year:2009 number:2 day:24 month:01 pages:299-311 https://dx.doi.org/10.1007/s00213-009-1460-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 204 2009 2 24 01 299-311 |
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Enthalten in Psychopharmacology 204(2009), 2 vom: 24. Jan., Seite 299-311 volume:204 year:2009 number:2 day:24 month:01 pages:299-311 |
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Enthalten in Psychopharmacology 204(2009), 2 vom: 24. Jan., Seite 299-311 volume:204 year:2009 number:2 day:24 month:01 pages:299-311 |
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GABA receptor subunit Stress-induced hyperthermia Body temperature βCCt zolpidem TP003 |
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Vinkers, Christiaan H. @@aut@@ Klanker, Marianne @@aut@@ Groenink, Lucianne @@aut@@ Korte, S. Mechiel @@aut@@ Cook, James M. @@aut@@ Van Linn, Michael L. @@aut@@ Hopkins, Seth C. @@aut@@ Olivier, Berend @@aut@@ |
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2009-01-24T00:00:00Z |
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Vinkers, Christiaan H. |
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Vinkers, Christiaan H. misc GABA misc receptor subunit misc Stress-induced hyperthermia misc Body temperature misc βCCt misc zolpidem misc TP003 Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
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Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress GABA (dpeaa)DE-He213 receptor subunit (dpeaa)DE-He213 Stress-induced hyperthermia (dpeaa)DE-He213 Body temperature (dpeaa)DE-He213 βCCt (dpeaa)DE-He213 zolpidem (dpeaa)DE-He213 TP003 (dpeaa)DE-He213 |
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misc GABA misc receptor subunit misc Stress-induced hyperthermia misc Body temperature misc βCCt misc zolpidem misc TP003 |
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misc GABA misc receptor subunit misc Stress-induced hyperthermia misc Body temperature misc βCCt misc zolpidem misc TP003 |
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misc GABA misc receptor subunit misc Stress-induced hyperthermia misc Body temperature misc βCCt misc zolpidem misc TP003 |
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Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
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(DE-627)SPR00201081X (SPR)s00213-009-1460-4-e |
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Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
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Vinkers, Christiaan H. |
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Psychopharmacology |
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2009 |
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Vinkers, Christiaan H. Klanker, Marianne Groenink, Lucianne Korte, S. Mechiel Cook, James M. Van Linn, Michael L. Hopkins, Seth C. Olivier, Berend |
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204 |
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Elektronische Aufsätze |
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Vinkers, Christiaan H. |
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10.1007/s00213-009-1460-4 |
| title_sort |
dissociating anxiolytic and sedative effects of $ gaba_{a} $ergic drugs using temperature and locomotor responses to acute stress |
| title_auth |
Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
| abstract |
Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. © The Author(s) 2009 |
| abstractGer |
Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. © The Author(s) 2009 |
| abstract_unstemmed |
Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. In conclusion, we show that home cage temperature and locomotor responses to novel home cage stress provide an excellent tool to assess both anxiolytic and sedative effects of various (subunit-selective) $ GABA_{A} $ergic compounds. © The Author(s) 2009 |
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Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR00201081X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519214123.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201001s2009 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s00213-009-1460-4</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR00201081X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s00213-009-1460-4-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Vinkers, Christiaan H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Dissociating anxiolytic and sedative effects of $ GABA_{A} $ergic drugs using temperature and locomotor responses to acute stress</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2009</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© The Author(s) 2009</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Rationale The stress-induced hyperthermia (SIH) model is an anxiety model that uses the transient rise in body temperature in response to acute stress. Benzodiazepines produce anxiolytic as well as sedative side effects through nonselective binding to $ GABA_{A} $ receptor subunits. The $ GABA_{A} $ receptor $ α_{1} $ subunit is associated with sedation, whereas the $ GABA_{A} $ receptor $ α_{2} $ and $ α_{3} $ subunits are involved in anxiolytic effects. Objectives We therefore examined the effects of (non)subunit-selective $ GABA_{A} $ receptor agonists on temperature and locomotor responses to novel cage stress. Results Using telemetric monitoring of temperature and locomotor activity, we found that nonsubunit-selective $ GABA_{A} $ receptor agonist diazepam as well as the $ α_{3} $ subunit-selective receptor agonist TP003 dose-dependently attenuated SIH and locomotor responses. Administration of $ GABA_{A} $ receptor $ α_{1} $-selective agonist zolpidem resulted in profound hypothermia and locomotor sedation. The $ GABA_{A} $ receptor $ α_{1} $-selective antagonist βCCt antagonized the hypothermia, but did not reverse the SIH response attenuation caused by diazepam and zolpidem. These results suggest an important regulating role for the $ α_{1} $ subunit in thermoregulation and sedation. Ligands of extrasynaptic $ GABA_{A} $ receptors such as alcohol and nonbenzodiazepine THIP attenuated the SIH response only at high doses. Conclusions The present study confirms a putative role for the $ GABA_{A} $ receptor $ α_{1} $ subunit in hypothermia and sedation and supports a role for $ α_{2/3} $ subunit $ GABA_{A} $ receptor agonists in anxiety processes. 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