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

doi:10.1016/0006-8993(93)91200-C

Alcohol modulation of cloned GABA_A 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

Medicine, Cardiology Division

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

The effects of n-octanol on GABA-induced currents were examined on the α₁β₂γ_2s and α₁β₂ combinations GABA_A 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 α₁β₂γ_2s 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 α₁β₂γ_2s combination only. We conclude that the potentiation of GABA_A receptor-mediated currents by a long carbon chain n-alcohol does not require the γ₂ subunit.

Original language	English (US)
Pages (from-to)	143-146
Number of pages	4
Journal	Brain research
Volume	631
Issue number	1
DOIs	https://doi.org/10.1016/0006-8993(93)91200-C
State	Published - 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

Access to Document

10.1016/0006-8993(93)91200-C

Cite this

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title = "Alcohol modulation of cloned GABAA receptor-channel complex expressed in human kidney cell lines",

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.",

keywords = "Alcohol, Benzodiazepine, Cloned GABA receptor, GABA subunit, Human kidney cell line, Octanol, γ-Aminobutyric acid",

author = "Yasutaka Kurata and William Marszalec and Hamilton, {Beverly J.} and Carter, {Donald B.} and Toshio Narahashi",

year = "1993",

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AU - Marszalec, William

AU - Hamilton, Beverly J.

AU - Carter, Donald B.

AU - Narahashi, Toshio

PY - 1993/12/17

Y1 - 1993/12/17

N2 - 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.

AB - 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.

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KW - Benzodiazepine

KW - Cloned GABA receptor

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KW - Human kidney cell line

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KW - γ-Aminobutyric acid

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