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Verfasst von:Jarolimek, Wolfgang [VerfasserIn]   i
 Misgeld, Ulrich [VerfasserIn]   i
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

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