How does alcohol impair neuronal migration?
J Neurosci Res
; 85(3): 465-70, 2007 Feb 15.
Article
em En
| MEDLINE
| ID: mdl-17139684
ABSTRACT
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 Ca(2+) 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.
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Base de dados:
MEDLINE
Assunto principal:
Etanol
/
Alcoolismo
/
Transtornos do Espectro Alcoólico Fetal
/
Neurônios
Tipo de estudo:
Prognostic_studies
Limite:
Child
/
Female
/
Humans
/
Pregnancy
Idioma:
En
Ano de publicação:
2007
Tipo de documento:
Article