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- W2035168085 abstract "Transient exposure to ethanol (EtOH) results in a massive neurodegeneration in the developing brain leading to behavioral and cognitive deficits observed in fetal alcohol syndrome. There is now compelling evidence that K+ channels play an important role in the control of programmed cell death. The aim of the present work was to investigate the involvement of K+ channels in the EtOH-induced cerebellar granule cell death and/or survival. At low and high concentrations, EtOH evoked membrane depolarization and hyperpolarization, respectively. Bath perfusion of EtOH (10 mM) depressed the IA (transient K+ current) potassium current whereas EtOH (400 mM) provoked a marked potentiation of the specific IK (delayed rectifier K+ current) current. Pipette dialysis with GTPγS or GDPβS did not modify the effects of EtOH (400 mM) on both membrane potential and IK current. In contrast, the reversible depolarization and slowly recovering inhibition of IA induced by EtOH (10 mM) became irreversible in the presence of GTPγS. EtOH (400 mM) induced prodeath responses whereas EtOH (10 mM) and K+ channel blockers promoted cell survival. Altogether, these results indicate that in cerebellar granule cells, EtOH mediates a dual effect on K+ currents partly involved in the control of granule cell death." @default.
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- W2035168085 date "2009-08-01" @default.
- W2035168085 modified "2023-10-02" @default.
- W2035168085 title "Paradoxical effect of ethanol on potassium channel currents and cell survival in cerebellar granule neurons" @default.
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- W2035168085 doi "https://doi.org/10.1111/j.1471-4159.2009.06197.x" @default.
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