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The Presence of Background Dopamine Signal Converts Long-Term Synaptic Depression to Potentiation in Rat Prefrontal Cortex

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84077

Marzo,  A
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Matsuda, Y., Marzo, A., & Otani, S. (2006). The Presence of Background Dopamine Signal Converts Long-Term Synaptic Depression to Potentiation in Rat Prefrontal Cortex. Journal of Neuroscience, 26(18), 4803-4810. doi:10.1523/​JNEUROSCI.5312-05.2006.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-D1DB-3
Abstract
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 D1 and D2 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.