Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings
Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We fou...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Samengo, Irene A. [verfasserIn] Scotti, Valerio [verfasserIn] Martire, Maria [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Journal of neural transmission - Wien [u.a.] : Springer, 1950, 120(2013), 12 vom: 03. Juli, Seite 1641-1649 |
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| Übergeordnetes Werk: |
volume:120 ; year:2013 ; number:12 ; day:03 ; month:07 ; pages:1641-1649 |
| Links: |
|---|
| DOI / URN: |
10.1007/s00702-013-1057-2 |
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| Katalog-ID: |
SPR007696671 |
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| 245 | 1 | 0 | |a Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
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| 520 | |a Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. | ||
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| 650 | 4 | |a and mGlu receptors |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a L-CCG-I |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a GABA release |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Cerebral cortex |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Scotti, Valerio |e verfasserin |4 aut | |
| 700 | 1 | |a Martire, Maria |e verfasserin |4 aut | |
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10.1007/s00702-013-1057-2 doi (DE-627)SPR007696671 (SPR)s00702-013-1057-2-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Samengo, Irene A. verfasserin aut Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 Scotti, Valerio verfasserin aut Martire, Maria verfasserin aut Enthalten in Journal of neural transmission Wien [u.a.] : Springer, 1950 120(2013), 12 vom: 03. Juli, Seite 1641-1649 (DE-627)300185901 (DE-600)1481655-6 1435-1463 nnns volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 https://dx.doi.org/10.1007/s00702-013-1057-2 lizenzpflichtig 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_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_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_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 44.90 ASE AR 120 2013 12 03 07 1641-1649 |
| spelling |
10.1007/s00702-013-1057-2 doi (DE-627)SPR007696671 (SPR)s00702-013-1057-2-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Samengo, Irene A. verfasserin aut Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 Scotti, Valerio verfasserin aut Martire, Maria verfasserin aut Enthalten in Journal of neural transmission Wien [u.a.] : Springer, 1950 120(2013), 12 vom: 03. Juli, Seite 1641-1649 (DE-627)300185901 (DE-600)1481655-6 1435-1463 nnns volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 https://dx.doi.org/10.1007/s00702-013-1057-2 lizenzpflichtig 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_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_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_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 44.90 ASE AR 120 2013 12 03 07 1641-1649 |
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10.1007/s00702-013-1057-2 doi (DE-627)SPR007696671 (SPR)s00702-013-1057-2-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Samengo, Irene A. verfasserin aut Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 Scotti, Valerio verfasserin aut Martire, Maria verfasserin aut Enthalten in Journal of neural transmission Wien [u.a.] : Springer, 1950 120(2013), 12 vom: 03. Juli, Seite 1641-1649 (DE-627)300185901 (DE-600)1481655-6 1435-1463 nnns volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 https://dx.doi.org/10.1007/s00702-013-1057-2 lizenzpflichtig 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_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_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_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 44.90 ASE AR 120 2013 12 03 07 1641-1649 |
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10.1007/s00702-013-1057-2 doi (DE-627)SPR007696671 (SPR)s00702-013-1057-2-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Samengo, Irene A. verfasserin aut Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 Scotti, Valerio verfasserin aut Martire, Maria verfasserin aut Enthalten in Journal of neural transmission Wien [u.a.] : Springer, 1950 120(2013), 12 vom: 03. Juli, Seite 1641-1649 (DE-627)300185901 (DE-600)1481655-6 1435-1463 nnns volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 https://dx.doi.org/10.1007/s00702-013-1057-2 lizenzpflichtig 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_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_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_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 44.90 ASE AR 120 2013 12 03 07 1641-1649 |
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10.1007/s00702-013-1057-2 doi (DE-627)SPR007696671 (SPR)s00702-013-1057-2-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Samengo, Irene A. verfasserin aut Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 Scotti, Valerio verfasserin aut Martire, Maria verfasserin aut Enthalten in Journal of neural transmission Wien [u.a.] : Springer, 1950 120(2013), 12 vom: 03. Juli, Seite 1641-1649 (DE-627)300185901 (DE-600)1481655-6 1435-1463 nnns volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 https://dx.doi.org/10.1007/s00702-013-1057-2 lizenzpflichtig 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_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_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_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 44.90 ASE AR 120 2013 12 03 07 1641-1649 |
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Enthalten in Journal of neural transmission 120(2013), 12 vom: 03. Juli, Seite 1641-1649 volume:120 year:2013 number:12 day:03 month:07 pages:1641-1649 |
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GABA and mGlu receptors Baclofen L-CCG-I GABA release Synaptosomes Cerebral cortex |
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Samengo, Irene A. @@aut@@ Scotti, Valerio @@aut@@ Martire, Maria @@aut@@ |
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G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">GABA</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">and mGlu receptors</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Baclofen</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">L-CCG-I</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">GABA release</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Synaptosomes</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cerebral cortex</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Scotti, Valerio</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Martire, Maria</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of neural transmission</subfield><subfield code="d">Wien [u.a.] : Springer, 1950</subfield><subfield code="g">120(2013), 12 vom: 03. 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Samengo, Irene A. |
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Samengo, Irene A. ddc 610 bkl 44.90 misc GABA misc and mGlu receptors misc Baclofen misc L-CCG-I misc GABA release misc Synaptosomes misc Cerebral cortex Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
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610 ASE 44.90 bkl Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings GABA (dpeaa)DE-He213 and mGlu receptors (dpeaa)DE-He213 Baclofen (dpeaa)DE-He213 L-CCG-I (dpeaa)DE-He213 GABA release (dpeaa)DE-He213 Synaptosomes (dpeaa)DE-He213 Cerebral cortex (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc GABA misc and mGlu receptors misc Baclofen misc L-CCG-I misc GABA release misc Synaptosomes misc Cerebral cortex |
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ddc 610 bkl 44.90 misc GABA misc and mGlu receptors misc Baclofen misc L-CCG-I misc GABA release misc Synaptosomes misc Cerebral cortex |
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ddc 610 bkl 44.90 misc GABA misc and mGlu receptors misc Baclofen misc L-CCG-I misc GABA release misc Synaptosomes misc Cerebral cortex |
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Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
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Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
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Samengo, Irene A. |
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Journal of neural transmission |
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Samengo, Irene A. Scotti, Valerio Martire, Maria |
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Samengo, Irene A. |
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co-application of the $ gaba_{b} $ receptor agonist, baclofen, and the mglu receptor agonist, l-ccg-i, facilitates [3h]gaba release from rat cortical nerve endings |
| title_auth |
Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
| abstract |
Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. |
| abstractGer |
Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. |
| abstract_unstemmed |
Abstract Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors’ ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the $ GABA_{B} $ agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [3H]GABA via a mechanism that involves mobilization of intracellular $ Ca^{2+} $ ions. The effect of L-CCG-I + baclofen was abolished by the phospholipase C inhibitor U73122, reduced by Xestospongin C (an IP3 receptor blocker), and blocked by 2-APB, an $ IP_{3} $ receptor antagonist. Pretreatment of the synaptosomes with the lipid-soluble $ Ca^{2+} $ chelator BAPTA-AM also inhibited the effects of L-CCG-I + baclofen. Subtype-selective non-competitive group I mGlu receptor antagonists, MPEP and CPCCOEt, had no effect on the release enhancement produced by baclofen + L-CCG-I. The enhancement was reversed by the $ GABA_{B} $ receptor antagonist, CGP54626, and by the group I/group II mGlu receptor antagonist (R,S)-MCPG. The GABA release-enhancing effects of L-CCG-I + baclofen in our model might reflect the presence on cortical nerve endings of $ GABA_{B} $/group I mGlu receptor heteromers with pharmacological properties distinct from those of the component receptors. Activation of these heteromeric receptors might modify the function of the $ GABA_{B} $ receptor in such a way that it facilitates GABAergic transmission, an effect that might be useful under conditions of excessive glutamatergic activity. |
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Co-application of the $ GABA_{B} $ receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [3H]GABA release from rat cortical nerve endings |
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| score |
7.3995953 |