Status: Bibliographieeintrag
Standort: ---
Exemplare:
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| Online-Ressource |
Verfasst von: | Jarolimek, Wolfgang [VerfasserIn]  |
| Misgeld, Ulrich [VerfasserIn]  |
Titel: | GABAB receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells |
Verf.angabe: | Wolfgang Jarolimek and Ulrich Misgeld |
E-Jahr: | 1997 |
Jahr: | 1 February 1997 |
Umfang: | 8 S. |
Teil: | volume:17 |
| year:1997 |
| number:3 |
| pages:1025-1032 |
| extent:8 |
Fussnoten: | Im Text ist das letzte "B" von GABAB tiefgestellt ; Gesehen am 27.04.2021 |
Titel Quelle: | Enthalten in: The journal of neuroscience |
Ort Quelle: | Washington, DC : Soc., 1981 |
Jahr Quelle: | 1997 |
Band/Heft Quelle: | 17(1997), 3, Seite 1025-1032 |
ISSN Quelle: | 1529-2401 |
Abstract: | Tight-seal whole-cell recordings from CA1 pyramidal cells of rodent hippocampus were performed to study GABAB receptor-mediated inhibition of tetrodotoxin (TTX)-resistant IPSCs. IPSCs were recorded in the presence of TTX and glutamate receptor antagonists. (R)-(−)-baclofen reduced the frequency of TTX-resistant IPSCs by a presynaptic action. The inhibition by (R)-(−)-baclofen was concentration-dependent, was not mimicked by the less effective enantiomer (S)-(+)-baclofen, and was blocked by the GABAB receptor antagonist CGP 55845A, suggesting a specific effect on GABAB receptors. The inhibition persisted in the presence of the Ca2+ channel blocker Cd2+. There was no requirement for an activation of K+conductances by (R)-(−)-baclofen, because the inhibition of TTX-resistant IPSCs persisted in Ba2+ and Cd2+. Because the time courses of TTX-resistant IPSCs were not changed by (R)-(−)-baclofen, there was no evidence for a selective inhibition of quantal release from a subgroup of GABAergic terminals. (R)-(−)-baclofen reduced the frequency of TTX-resistant IPSCs in guinea pigs and Wistar rats, whereas the inhibition was much smaller in Sprague Dawley rats. In Cd2+ and Ba2+, β-phorbol-12,13-dibutyrate and forskolin enhanced the frequency of TTX-resistant IPSCs. Only β-phorbol-12,13-dibutyrate reduced the inhibition by (R)-(−)-baclofen. We conclude that GABABreceptors inhibit TTX-resistant GABA release through a mechanism independent from the well known effects on Ca2+ or K+ channels. The inhibition of quantal GABA release can be reduced by an activator of protein kinase C. |
DOI: | doi:10.1523/JNEUROSCI.17-03-01025.1997 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext ; Verlag: https://doi.org/10.1523/JNEUROSCI.17-03-01025.1997 |
| Volltext: https://www.jneurosci.org/content/17/3/1025 |
| DOI: https://doi.org/10.1523/JNEUROSCI.17-03-01025.1997 |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | adenylate cyclase |
| baclofen |
| GABA |
| GABAB receptors |
| miniature IPSCs |
| presynaptic |
| protein kinase C |
| quantal release |
K10plus-PPN: | 1756003939 |
Verknüpfungen: | → Zeitschrift |
GABAB receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells / Jarolimek, Wolfgang [VerfasserIn]; 1 February 1997 (Online-Ressource)
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