Short communicationα7 Nicotinic receptor-mediated protection against ethanol-induced oxidative stress and cytotoxicity in PC12 cells
Section snippets
Acknowledgements
We thank Neal Benton of the University of Florida ICBR for his expert technical support with the flow cytometry, and Dr. John Shryock for helpful discussions of the manuscript. This work was supported in part by T32 AA07561, NIH PO1 10485 and NIAAA RO1 AA 11597.
References (25)
- et al.
Nicotine-induced protection of cultured cortical neurons against N-methyl-d-aspartate receptor-mediated glutamate cytotoxicity
Brain Res.
(1994) - et al.
Hydrogen peroxide mediates amyloid β protein toxicity
Cell
(1994) - et al.
α7 nicotinic receptor mediated protection against ethanol-induced cytocoxicity in PC12 cells
Brain Res.
(1999) - et al.
Characterization of the neuroprotective and toxic effects of α7 nicotinic receptor activation in PC12 cells
Brain Res.
(1999) - et al.
[2,4-dimethoxybenzylidene]anabaseine (DMXB) selectively activates rat receptors and improves memory-related behaviors in a mecamylamine-sensitive manner
Brain Res.
(1997) - et al.
Implication of free radical mechanisms in ethanol-induced cellular injury
Free Rad. Biol. Med.
(1992) - et al.
Evaluation of 2,7 dichlorofluorescin and dihydrorhodamine 123 as fluorescent probes for intracellular H2O2 in cultured endothelial cells
Arch. Biochem. Biophys.
(1993) - et al.
Alpha7 nicotinic receptor activation protects against NMDA-induced toxicity in vitro and focal ischemia induced neurotoxicity
Brain Res.
(1998) - et al.
Blockade of nicotinic currents in hippocampal neurons defines methyllycaconitine as a potent and specific receptor antagonist
Mol. Pharmacol.
(1992) - et al.
Ethanol promotes apoptosis in cerebellar granule cells by inhibiting the trophic effect of NMDA
J. Neurochem.
(1997)
Detection of functional nicotinic receptors blocked by α-bungarotoxin on PC12 cells and dependence of their expression on post-translational events
J. Neurosci.
Alterations of excitatory amino acid receptors in the brain of manganese-treated mice
Mol. Chem. Neuropathol.
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2011, Reproductive and Developmental ToxicologyIs fipronil safer than chlorpyrifos? Comparative developmental neurotoxicity modeled in PC12 cells
2009, Brain Research BulletinCitation Excerpt :One possible explanation is a slowing of the cell loss that occurs through apoptosis as a normal consequence of neurodifferentiation [24,73]. Stimulation of nicotinic acetylcholine receptors provides an effective antiapoptotic signal, both in PC12 cells [40,68,79,86] and in the brain in vivo [8,37,43,57]. Here, we found that FPN enhanced PC12 cell differentiation into the acetylcholine phenotype, which might thus provide an antiapoptotic signal that results in maintenance of cells that otherwise would be fated to die.