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  • Title: Prolonged exposure to gamma-aminobutyric acid up-regulates stably expressed recombinant alpha 1 beta 2 gamma 2s GABAA receptors.
    Author: Pericić D, Strac DS, Jembrek MJ, Rajcan I.
    Journal: Eur J Pharmacol; 2003 Dec 15; 482(1-3):117-25. PubMed ID: 14660012.
    Abstract:
    The aim of this study was to better understand the mechanisms that underlie adaptive changes in GABA(A) receptors following their prolonged exposure to drugs. Exposure (48 and/or 96 h) of human embryonic kidney (HEK 293) cells stably expressing recombinant alpha1beta2gamma2s GABA(A) receptors for gamma-aminobutyric (GABA, 1 mM) and muscimol (100 microM), but not for diazepam (1 microM), enhanced the maximum number (B(max)) of [3H]flunitrazepam binding sites without affecting their affinity (K(d)). The GABA-induced enhancement in B(max) was reduced by the GABA receptor antagonist, bicuculline (100 microM), and by cycloheximide (10 microl/ml), a protein synthesis inhibitor. GABA (100 microM) enhanced the affinity of [3H]flunitrazepam binding to vehicle- and GABA-pretreated, but not to diazepam-pretreated, HEK 293 cells. The results suggest that chronic GABA treatment up-regulates stably expressed GABA(A) receptors, presumably by stimulating their synthesis. Unlike chronic diazepam, which produced functional uncoupling of GABA and benzodiazepine binding sites, chronic GABA failed to produce this effect.
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