Isoflurane slows inactivation kinetics of rat recombinant α1β2γ2L GABAA receptors: Enhancement of GABAergic transmission despite an open-channel block

Gerhard Hapfelmeier, Rainer Haseneder, Matthias Eder, Helmuth Adelsberger, Eberhard Kochs, Gerhard Rammes, Walter Zieglgänsberger

Publikation: Beitrag in FachzeitschriftArtikelBegutachtung

15 Zitate (Scopus)

Abstract

Recombinant α1β2γ2L γ-aminobutyric acid (A) receptor (GABAAR) channels expressed in human embryonic kidney (HEK293) cells were used for patch-clamp experiments. The currents activated by brief pulses of GABA (10-4 M) applied with a device for fast solution exchange to cells clamped in the whole-cell configuration mimicked GABAAR-mediated inhibitory postsynaptic currents. Isoflurane (ISO) at clinically relevant concentrations (0.6 mM) decreased the amplitude and prolonged the decay of the GABA-evoked response. To further detail the mechanism underlying the prolonged decay time, we made simulations based on these measurements. These simulations suggest that ISO slows the rate of GABA unbinding from the receptor. Under these conditions, ISO increases the GABA-induced charge transfer and, thus, could enhance GABAergic inhibition despite the concomitant open-channel block causing the decrease in the current amplitude.

OriginalspracheEnglisch
Seiten (von - bis)97-100
Seitenumfang4
FachzeitschriftNeuroscience Letters
Jahrgang307
Ausgabenummer2
DOIs
PublikationsstatusVeröffentlicht - 13 Juli 2001

Fingerprint

Untersuchen Sie die Forschungsthemen von „Isoflurane slows inactivation kinetics of rat recombinant α1β2γ2L GABAA receptors: Enhancement of GABAergic transmission despite an open-channel block“. Zusammen bilden sie einen einzigartigen Fingerprint.

Dieses zitieren