GABAB receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells

• Verfasst von: Jarolimek, Wolfgang [VerfasserIn]
• Verfasst von: 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
• Teil: year:1997
• Teil: number:3
• Teil: pages:1025-1032
• Teil: 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
• DOI: doi:10.1523/JNEUROSCI.17-03-01025.1997
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: adenylate cyclase
• Sach-SW: baclofen
• Sach-SW: GABA
• Sach-SW: GABAB receptors
• Sach-SW: miniature IPSCs
• Sach-SW: presynaptic
• Sach-SW: protein kinase C
• Sach-SW: quantal release
• K10plus-PPN: 1756003939

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.