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Review
. 2011 Jun;17(3):274-87.
doi: 10.1177/1073858410383336. Epub 2011 Mar 7.

Fetal alcohol spectrum disorders and abnormal neuronal plasticity

Alexandre E Medina  1
Affiliations
Review

Fetal alcohol spectrum disorders and abnormal neuronal plasticity

Alexandre E Medina. Neuroscientist. 2011 Jun.

Abstract

The ingestion of alcohol during pregnancy can result in a group of neurobehavioral abnormalities collectively known as fetal alcohol spectrum disorders (FASD). During the past decade, studies using animal models indicated that early alcohol exposure can dramatically affect neuronal plasticity, an essential property of the central nervous system responsible for the normal wiring of the brain and involved in processes such as learning and memory. The abnormalities in neuronal plasticity caused by alcohol can explain many of the neurobehavioral deficits observed in FASD. Conversely, improving neuronal plasticity may have important therapeutic benefits. In this review, the author discuss the mechanisms that lead to these abnormalities and comment on recent pharmacological approaches that have been showing promising results in improving neuronal plasticity in FASD.

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Conflict of interest statement

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interests with respect to the authorship and/or publication of this article.

Figures

Figure 3
Figure 3
Activation of the CREB/serum response factor (SRF), a crucial cascade for neuronal plasticity. It has been demonstrated that vinpocetine, aniracetam, and choline have successfully improved neuronal plasticity in models of fetal alcohol spectrum disorder (FASD) by different mechanisms. Vinpocetine, as a phosphodiesterase (PDE) type 1 inhibitor, increases levels of cAMP and cGMP. Aniracetam, as an AMPA receptor modulator, facilitates glutamatergic transmission. Although its specific mechanism is poorly understood, it is known that there is a correlation between choline supplementation and facilitation of NMDA function and an increase in phosphorylation of ERK and CREB.
Figure 1
Figure 1
Typical facial features observed in fetal alcohol syndrome.
Figure 2
Figure 2
Alcohol-triggered apoptosis revealed by Fluoro-Jade B staining 24 hours after ethanol exposure (5 g/kg subcutaneously). Modified from Ieraci and Herrera (2006). PLoS One, open access.
See this image and copyright information in PMC

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