How does alcohol impair neuronal migration?

Maternal alcohol consumption during pregnancy can cause serious birth defects, of which fetal alcohol syndrome (FAS) is the most devastating. Recognized by characteristic craniofacial abnormalities and growth deficiency, this condition produces severe alcohol‐induced damage in the developing brain....

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Bibliographic Details
Published in:Journal of neuroscience research 2007-02, Vol.85 (3), p.465-470
Main Authors: Kumada, Tatsuro, Jiang, Yulan, Cameron, D. Bryant, Komuro, Hitoshi
Format: Article
Language:English
Subjects:
Alcoholism - physiopathology
Ca2+ signaling
Calcium Signaling
cAMP-PKA signaling
Cell Movement - drug effects
cerebellar granule cells
Cerebellum - growth & development
cGMP-PKG signaling
Child
Cytoplasmic Granules - drug effects
Cytoplasmic Granules - physiology
Ethanol - pharmacology
Female
Fetal Alcohol Spectrum Disorders - etiology
fetal alcohol syndrome
Humans
Models, Biological
Neurons - drug effects
Neurons - physiology
Nucleotides, Cyclic - physiology
Pregnancy
Signal Transduction - drug effects
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Summary:Maternal alcohol consumption during pregnancy can cause serious birth defects, of which fetal alcohol syndrome (FAS) is the most devastating. Recognized by characteristic craniofacial abnormalities and growth deficiency, this condition produces severe alcohol‐induced damage in the developing brain. FAS children experience ataxia; deficits in intellectual functioning; and difficulties in learning, memory, problem solving, and attention. Multiple aspects of central nervous system development can be affected by alcohol exposure, but the most striking abnormalities are neuronal and glial migration. Little is known about cellular mechanisms by which alcohol affects the migration of immature neurons. Recently, it has been found that Ca2+ signaling and cyclic nucleotide signaling are the central targets of the action of alcohol in neuronal cell migration. Most importantly, the aberrant migration of immature neurons caused by alcohol exposure is significantly ameliorated by controlling the activity of these second‐messenger pathways. In this Mini‐Review, we first describe how alcohol exposure impairs the migration of cerebellar granule cells and then discuss the signaling mechanisms involved. © 2006 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.21149