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Friday, May 30, 2008

Postnatal binge-like alcohol exposure reduces spine density without affecting dendritic morphology in rat mPFC
Synapse 62:566-573, 2008.


Among the deficits associated with fetal alcohol syndrome (FAS), cognitive impairments are the most debilitating and permanent. These impairments, including deficits in goal-directed behavior, attention, temporal planning, and other executive functions, could result from damage to the prefrontal cortex (PFC), an area that has not been studied sufficiently in the context of FAS.

Neuronal connectivity in this area, as measured by distribution of dendritic spines and the complexity of dendritic tree structure, can be influenced by exogenous variables other than alcohol, and the neuronal connectivity in other brain regions can be affected by alcohol exposure.

The goal of this study was to determine whether binge-like alcohol exposure on postnatal days (PD) 4-9 affects dendritic spine density and other dendritic tree parameters in mPFC that could possibly underlie functional damage.

Spine density was significantly decreased in AE animals relative to SI and SC controls, but no differences in dendritic complexity were found across experimental groups.

Our findings demonstrate that neonatal alcohol exposure has a persistent effect on the spine density in mPFC that can explain functional deficits in this cortical area.


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Request Reprint E-Mail: klintsov@udel.edu
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