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., 2004). Higher concentrations of dopamine lead to suppression of interneuron excitability via a D2-receptor-mediated pathway that leads to enhanced phosphatase activity and reduced release of GABA (Trantham-Davidson et al., 2004, 2008). In a recent study that utilized the slice culture model described above, Kroener et al. (2009) investigated the impact of dopamine on persistent activity of deep-layer pyramidal neurons. These cultures contained slices of PFC and VTA, and dopaminergic neurons established a strong innervation of the PFC slice consistent with that observed in vivo. Adding 1 uM or more exogenous dopamine reduced up-state duration and spiking activity whereas dopamine enhanced up-state duration and firing in cultures lacking endogenous DA tone. Action potentials induced by direct current injection during down-state periods were enhanced by dopamine even at concentrations as low as 100nM. Dopamine also enhanced the ability of stimulus-evoked EPSPs to induce firing when these events were generated during an up-state. This effect was concentration dependent as up-state duration and spiking
