GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in rat midbrain culture.

• Verfasst von: Rohrbacher, Jutta [VerfasserIn]
• Verfasst von: Jarolimek, Wolfgang [VerfasserIn]
• Verfasst von: Lewen, Andrea [VerfasserIn]
• Verfasst von: Misgeld, Ulrich [VerfasserIn]
• Titel: GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in rat midbrain culture.
• Verf.angabe: Jutta Rohrbacher, Wolfgang Jarolimek, Andrea Lewen and Ulrich Misgeld
• E-Jahr: 1997
• Jahr: 01 May 1997
• Umfang: 11 S.
• Teil: volume:500
• Teil: year:1997
• Teil: number:3
• Teil: pages:739-749
• Teil: extent:11
• Fussnoten: ImText ist das letzte "B" von GABAB tiefgestellt ; Gesehen am 27.04.2021
• Titel Quelle: Enthalten in: The journal of physiology
• Ort Quelle: Hoboken, NJ : Wiley-Blackwell, 1878
• Jahr Quelle: 1997
• Band/Heft Quelle: 500(1997), 3, Seite 739-749
• ISSN Quelle: 1469-7793
• DOI: doi:10.1113/jphysiol.1997.sp022055
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1756005575

Abstract

1. Tight-seal, whole-cell recording was used to study GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in cultured rat midbrain neurones. 2. Spontaneous miniature inhibitory postsynaptic currents (mIPSCs) were recorded in tetrodotoxin (TTX), Cd2+ and Ba2+. (R)-(-)-baclofen reduced the frequency of mIPSCs through a presynaptic mechanism. The EC50 for this effect was 7 microM. It was antagonized by the GABAB receptor antagonist CGP55845A (0.5 microM). 3. In pertussis toxin (PTX)-treated cultures, some GABAB receptor-mediated reduction of the frequency of mIPSCs persisted. In contrast, PTX treatment totally abolished inhibition of miniature excitatory postsynaptic currents (mEPSCs). 4. In PTX-treated cultures, a saturating concentration of (R)-(-)-baclofen inhibited action potential-generated IPSCs but no EPSCs. 5. PTX treatment abolished the (R)-(-)-baclofen-mediated inhibition of high voltage-activated somatic Ca2+ currents and of spontaneous IPSCs depending on presynaptic Ca2+ entry. 6. We conclude that cellular mechanisms underlying GABAB receptor-mediated inhibition of mIPSCs contribute to auto-inhibition of GABA release.