This week, two groups look at impairments of neuronal migration and synaptic plasticity, respectively, in animal models of fetal alcohol syndrome (FAS).
Both studies implicate cAMP signaling but in different ways. Kumada et al. examined granule cell migration in a brain slice preparation of neonatal mouse cerebellum.
The authors report that acute alcohol exposure slowed the migration of granule cells.
Medina et al. used a ferret model of FAS in which alcohol was injected every other day between postnatal days 10 and 30. Subsequently, ocular dominance plasticity was impaired in FAS animals, an effect that was restored by a phosphodiesterase I inhibitor.
Tatsuro Kumada, Madepalli K.Lakshmana, and Hitoshi Komuroand and Alexandre E. Medina, Thomas E. Krahe, and Ary S. Ramoa
Sara Harris
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Society for Neuroscience
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