L1 cell adhesion molecule is neuroprotective of alcohol induced cell death

• Published in: Neurotoxicology (Park Forest South) 2007-05, Vol.28 (3), p.457-462
• Main Authors: Gubitosi-Klug, Rose, Larimer, Corena G., Bearer, Cynthia F.
• Format: Article
• Language: English
• Subjects: Alcoholism and acute alcohol poisoning; Animals; Biological and medical sciences; Cell death; Cell Death - drug effects; Cell Survival - drug effects; Central Nervous System Depressants - toxicity; Cerebellar granule neurons; Cerebellum - cytology; Cerebellum - drug effects; Ethanol; Ethanol - toxicity; Fetal alcohol spectrum disorder; Fetal alcohol syndrome; Humans; L1 cell adhesion molecule; Medical sciences; Mice; Neural Cell Adhesion Molecule L1 - isolation & purification; Neural Cell Adhesion Molecule L1 - pharmacology; Neurites - drug effects; Neurites - ultrastructure; Neurons - drug effects; Neuroprotective Agents; NIH 3T3 Cells; Plasmids - genetics; Polylysine - pharmacology; Potassium Deficiency - pathology; Rats; Rats, Sprague-Dawley; Toxicology
• ISSN: 0161-813X; 1872-9711
• DOI: 10.1016/j.neuro.2006.11.008

L1 cell adhesion molecule (L1), a protein critical for appropriate development of the central nervous system, is a target for ethanol teratogenicity. Ethanol inhibits both L1 mediated cell adhesion as well as L1 mediated neurite outgrowth. L1 has been shown to increase cell survival in cerebellar granule cells while ethanol has been shown to increase cell death. We sought to determine if L1 protected cells from ethanol induced cell death. Cerebellar granule cells from postnatal day 6 rat pups were cultured on either poly l-lysine with or without an L1 substratum. Alcohol was added at 2 h post-plating and cell survival was measured at various times. L1 substratum significantly increased cell survival at 72 and 120 h. Ethanol significantly reduced cell survival at 48 h, with no effect at 72 or 120 h, both in the presence and absence of L1. At 48 h, L1 significantly increased cell survival in the presence of ethanol. We conclude that ethanol interferes with processes other than L1–L1 interactions in causing cell death, and that ethanol effects would be more severe in the absence of L1.