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

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

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.

Original languageEnglish
Pages (from-to)97-100
Number of pages4
JournalNeuroscience Letters
Volume307
Issue number2
DOIs
StatePublished - 13 Jul 2001
Externally publishedYes

Keywords

  • Anesthetics
  • Channel block
  • Computer simulations
  • Isoflurane
  • Patch-clamp
  • γ-Aminobutyric acid (A) receptor

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