Along with dendritic complexity, dendritic spines in the prefrontal cortex are also greatly influenced by external factorssuch as stress (Radley et al., 2008), dopamine depletion (Wang & Deutch, 2008) and alcohol exposure (Whitcher & Klintsova, 2008). A postnatal-binge like alcohol exposure has been shown to affect spine density without affecting the dendritic morphology of apical dendrites in Layer III pyramidal cells, suggesting that the plasticity of spines on PFC neurons may be most vulnerable to alcohol exposure at this developmental stage (Whitcher & Klintsova, 2008). This harmful effect of alcohol exposure on the highly plastic pyramidal neurons in a still developing cortex is evident in both humans and in rats. In 1987, Ferrer and Galofré described a case study of a 4-month-old male, diagnosed with FAS, who died of pneumonia. His autopsy revealed that there was a decrease in spine density on the apical Layer V pyramidal neurons in his PFC as well as an increase in immature spines. Alcohol exposure in rat pups during postnatal days 2–6 has been shown to affect cortical areas, such as primary somatosensory and
