Dopamine modulation of PFC function has long been known to be important for optimizing cognitive performance, especially in tasks requiring working memory. Disruption of this important modulatory input is associated with various neurological and psychiatric illnesses. PFC dopamine arises from terminals provided by dopaminergic neurons whose cell bodies reside in the ventral tegmental area (VTA). These neurons also provide dopaminergic tone to other limbic structures including nucleus accumbens and recent evidence suggests that there are discrete subpopulations of VTA dopamine neurons that display both anatomical and functional specializations depending on their pattern of innervation (Lammel et al., 2008). There is a rich literature regarding the effects of dopamine on PFC-associated behaviors and neuronal function and the reader is referred to several excellent reviews of this material (Tzschentke, 2001; Seamans and Yang, 2004). A brief summary of the key findings as they relate to PFC electrophysiology is presented here. In the prefrontal cortex, dopamine D1 receptors are expressed to a higher degree than other subtypes and are located primarily on dendritic spines and shafts of target neurons. D2 dopamine receptors are
