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).

Postnatal binge-like alcohol exposure reduces spine density without affecting dendritic morphology in rat mPFC.

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.