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• W2123233316 abstract "Diverse γ-aminobutyric acid (GABA A ) receptor modulators exhibited novel cytoprotective effects and mechanisms of action in rabbit renal proximal tubules subjected to mitochondrial inhibition (antimycin A) or hypoxia. Cytoprotective potencies (50% effective concentration, EC 50 ) were 0.3 nM allopregnanolone (AP) > 0.4 nM 17α-OH-allopregnanolone (17α-OH-AP) > 30 nM dehydroepiandrosterone sulfate (DHEAS) = 30 nM pregnenolone sulfate (PS) > 500 nM pregnenolone (PREG) > 30 μM muscimol > 10 mM GABA following antimycin A exposure. Maximal protection with AP and 17α-OH-AP was 70%, whereas DHEAS, PS, PREG, and muscimol produced 100% cytoprotection. Experiments with AP, PS, and muscimol revealed the return of mitochondrial function and active Na + transport following hypoxia/reoxygenation. Muscimol inhibited the antimycin A-induced influx of both extracellular Ca 2+ and Cl − that occurs during the late phase of cell injury, whereas the neurosteroids only inhibited influx of Cl − . Radioligand binding studies with AP and PS did not reveal a specific binding site; however, structural requirements were observed for cytoprotective potency and efficacy. In conclusion, we suggest that the GABA A receptor modulators muscimol and neurosteroids are cytoprotective at different cellular sites in the late phase of cell injury; muscimol inhibits Ca 2+ and subsequent Cl − influx, whereas the neurosteroids inhibit Cl − influx." @default.
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• W2123233316 date "1997-12-01" @default.
• W2123233316 modified "2023-10-10" @default.
• W2123233316 title "Neurosteroid inhibition of cell death" @default.
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• W2123233316 doi "https://doi.org/10.1152/ajprenal.1997.273.6.f869" @default.
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