RGD Reference Report - Effects of ethanol on axon outgrowth and branching in developing rat cortical neurons. - Rat Genome Database

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Effects of ethanol on axon outgrowth and branching in developing rat cortical neurons.

Authors: Hoffman, EJ  Mintz, CD  Wang, S  McNickle, DG  Salton, SR  Benson, DL 
Citation: Hoffman EJ, etal., Neuroscience. 2008 Dec 2;157(3):556-65. doi: 10.1016/j.neuroscience.2008.08.071. Epub 2008 Sep 25.
RGD ID: 11570516
Pubmed: PMID:18926887   (View Abstract at PubMed)
PMCID: PMC2626542   (View Article at PubMed Central)
DOI: DOI:10.1016/j.neuroscience.2008.08.071   (Journal Full-text)

Humans exposed prenatally to ethanol can exhibit brain abnormalities and cognitive impairment similar to those seen in patients expressing mutant forms of the L1 cell adhesion molecule (L1CAM). The resemblance suggests that L1CAM may be a target for ethanol, and consistent with this idea, ethanol can inhibit L1CAM adhesion in cell lines and L1CAM-mediated outgrowth and signaling in cerebellar granule neurons. However, it is not known whether ethanol inhibits L1CAM function in other neuron types known to require L1CAM for appropriate development. Here we asked whether ethanol alters L1CAM function in neurons of the rat cerebral cortex. We find that ethanol does not alter axonal polarization, L1CAM-dependent axon outgrowth or branching, or L1CAM recycling in axonal growth cones. Thus, ethanol inhibition of L1CAM is highly dependent on neuronal context.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cellular response to ethanol NOTIEP 11570516 RGD 

Objects Annotated

Genes (Rattus norvegicus)
L1cam  (L1 cell adhesion molecule)


Additional Information