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 I(A) (transient K+ current) potassium current whereas EtOH (400 mM) provoked a marked potentiation of the specific I(K) (delayed rectifier K+ current) current. Pipette dialysis with GTPgammaS or GDPbetaS did not modify the effects of EtOH (400 mM) on both membrane potential and I(K) current. In contrast, the reversible depolarization and slowly recovering inhibition of I(A) induced by EtOH (10 mM) became irreversible in the presence of GTPgammaS. 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.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Lefebvre T,Gonzalez BJ,Vaudry D,Desrues L,Falluel-Morel A,Aubert N,Fournier A,Tonon MC,Vaudry H,Castel Hdoi
10.1111/j.1471-4159.2009.06197.xsubject
Has Abstractpub_date
2009-08-01 00:00:00pages
976-89issue
3eissn
0022-3042issn
1471-4159pii
JNC6197journal_volume
110pub_type
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