Prenatal exposure to alcohol in humans can result in a wide range of deficits collectively referred to as Fetal Alcohol Spectrum Disorders. Of these deficits, cognitive impairments are among the most debilitating and long-lasting. Specifically, cognitive impairments in executive functioning suggest damage to the prefrontal cortex (PFC). Several external stimuli, such as morphine, chronic stress and maternal stress have been found to alter the dendritic structure of cells within the PFC. In this study, three groups of rat pups were used: intubated with alcohol (5.25g/kg/day; AE), sham intubated (SI), or suckle controls (SC) on PD4-9. On PD26-30 rats were anesthetized, perfused with saline and brains were processed for Golgi-Cox staining. Basilar dendrite complexity, spine density and spine phenotypes were evaluated for Layer II/III neurons in the medial PFC. Results indicate that AE rats have an altered basilar dendritic tree complexity due to a significant decrease in both length and number of intersections in proximity to the neuronal soma. Furthermore, spine density patterns of basilar dendrites remain unchanged while the density of mature versus immature spines significantly changes. These effects were not seen in the apical dendrites, indicating alcohol’s influence on different neuronal parts in a single cell. In addition, these results suggest that the innervations of the soma and basilar dendrites by thalamic projections may play a role. Thus, our data demonstrates that postnatal exposure to alcohol produces changes in the neuronal organization of rat adolescent PFC that may affect the performance on prefrontal-dependant behavioral tasks.

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. Rats were intubated with alcohol [5.25 g/kg/day; alcohol exposed (AE)], sham intubated (SI), or remained with the mother (SC, suckle control) on PD 4-9. Animals were sacrificed between PD 26 and PD 30 and brains were processed for Golgi-Cox staining. Apical dendrite complexity and spine density were evaluated for layer III neurons in the mPFC using NeuroLucida software (MicroBrightField, Inc.). 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.