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Title: Ethanol causes the redistribution of L1 cell adhesion molecule in lipid rafts
Authors: Tang, N.
Farah, B.
He, M. 
Fox, S.
Malouf, A.
Littner, Y.
Bearer, C.F.
Keywords: cerebellar granule neurons
fetal alcohol spectrum disorder
L1 cell adhesion molecule
lipid rafts
neurite outgrowth
Issue Date: Nov-2011
Citation: Tang, N., Farah, B., He, M., Fox, S., Malouf, A., Littner, Y., Bearer, C.F. (2011-11). Ethanol causes the redistribution of L1 cell adhesion molecule in lipid rafts. Journal of Neurochemistry 119 (4) : 859-867. ScholarBank@NUS Repository.
Abstract: Fetal alcohol spectrum disorder is estimated to affect 1% of live births. The similarities between children with fetal alcohol syndrome and those with mutations in the gene encoding L1 cell adhesion molecule (L1) implicates L1 as a target of ethanol developmental neurotoxicity. Ethanol specifically inhibits the neurite outgrowth promoting function of L1 at pharmacologic concentrations. Emerging evidence shows that localized disruption of the lipid rafts reduces L1-mediated neurite outgrowth. We hypothesize that ethanol impairment of the association of L1 with lipid rafts is a mechanism underlying ethanol's inhibition of L1-mediated neurite outgrowth. In this study, we examine the effects of ethanol on the association of L1 and lipid rafts. We show that, in vitro, L1 but not N-cadherin shifts into lipid rafts following treatment with 25 mM ethanol. The ethanol concentrations causing this effect are similar to those inhibiting L1-mediated neurite outgrowth. Increasing chain length of the alcohol demonstrates the same cutoff as that previously shown for inhibition of L1-L1 binding. In addition, in cerebellar granule neurons in which lipid rafts are disrupted with methyl-beta-cyclodextrin, the rate of L1-mediated neurite outgrowth on L1-Fc is reduced to background rate and that this background rate is not ethanol sensitive. These data indicate that ethanol may inhibit L1-mediated neurite outgrowth by retarding L1 trafficking through a lipid raft compartment. © 2011 International Society for Neurochemistry.
Source Title: Journal of Neurochemistry
ISSN: 00223042
DOI: 10.1111/j.1471-4159.2011.07467.x
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