The presence of background dopamine signal converts long-term synaptic depression to potentiation in rat prefrontal cortex

Executive functions of the brain are believed to require tonic dopamine inputs to the prefrontal cortex ( PFC). It is unclear, however, how this background dopamine activity controls synaptic plasticity in the PFC, a possible underlying mechanism of executive functions. Using PFC slices, we show that pairing of dopamine with weak tetanic stimulation, a maneuver that otherwise induces NMDA receptor-independent long-term depression ( LTD), induces long-term potentiation ( LTP) when primed with dopamine. This priming occurs through the combined activation of D-1 and D-2 receptors and requires 12-40 min to develop. Moreover, concurrent synaptic activation of NMDA receptors during priming is necessary for this novel form of LTP. We suggest that a role of background dopamine signals in the PFC is to prevent high-frequency synaptic inputs from abnormally inducing LTD and to secure the induction of LTP.