Alcohol modulation of cloned GABAA receptor-channel complex expressed in human kidney cell lines

Yasutaka Kurata, William Marszalec, Beverly J. Hamilton, Donald B. Carter, Toshio Narahashi*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

The effects of n-octanol on GABA-induced currents were examined on the α1β2γ2s and α1β2 combinations GABAA receptor subunits expressed in a human kidney cell line (HEK 293), using the whole-cell variation of the patch clamp technique. The EC50 of the GABA dose-response curve for the α1β2 combination was lower than that for the α1β2γ2s combination. n-Octanol at 100 μM augmented the GABA-induced currents in a dose-dependent manner, decreasing the EC50 of the GABA dose-response curve without affecting the maximal response. The magnitude of n-octanol potentiation was nearly the same in both combinations. In contrast, a benzodiazepine agonist, chlordiazepoxide, augmented the currents of the α1β2γ2s combination only. We conclude that the potentiation of GABAA receptor-mediated currents by a long carbon chain n-alcohol does not require the γ2 subunit.

Original languageEnglish (US)
Pages (from-to)143-146
Number of pages4
JournalBrain research
Volume631
Issue number1
DOIs
StatePublished - Dec 17 1993

Keywords

  • Alcohol
  • Benzodiazepine
  • Cloned GABA receptor
  • GABA subunit
  • Human kidney cell line
  • Octanol
  • γ-Aminobutyric acid

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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