Postnatal binge-like alcohol exposure decreases dendritic complexity while increasing the density of mature spines in mPFC Layer II/III pyramidal neurons.

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 (5.25 g/kg/day; AE), sham intubated (SI), or suckle controls (SC) on PD 4-9. On PD 26-30 rats were anesthetized, perfused with saline and brains were processed for Golgi-Cox staining. Basilar dendritic 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 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 vs. 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.