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 expressed both pre- and postsynaptically, and receptors on axon terminals reduce the release of both glutamate and GABA. In general, most studies have shown that dopamine transiently reduces neuronal excitability followed by a long-lasting enhancement in firing activity. These effects arise from both modulation of intrinsic mediators of excitability (voltage-sensitive Na+ and K+ channels) and changes in glutamatergic and GABAergic synaptic transmission. D1-mediated responses are associated primarily with a long-lasting increase in excitability, with NMDA currents being particularly sensitive to low concentrations of dopamine that potentiate NMDA EPSCs. At higher doses, dopamine and certain D1 agonists may actually inhibit NMDA function via direct channel blockade suggesting caution in interpreting results when high concentrations of these compounds are used (Cui et al., 2006). Dopamine also enhances the firing activity of fast-spiking but not other types of interneurons in the prefrontal cortex (Gorelova et al., 2002). This effect is blocked by D1 antagonists and involves the cAMP:PKA signaling pathway (Trantham-Davidson et al.,
