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The Journal of Neuroscience, May 3, 2006, 26(18):4803-4810; doi:10.1523/JNEUROSCI.5312-05.2006

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

Yoshiki Matsuda, Aude Marzo, and Satoru Otani

Laboratory of Neuromodulation, Neuronal Plasticity and Cognition, Centre National de la Recherche Scientifique-Unité Mixte de Recherche 7102 Neurobiologie des Processus Adaptatifs, Université Paris VI Pierre et Marie Curie, 75005 Paris, France

Correspondence should be addressed to Satoru Otani at the above address. Email: satoru.otani{at}snv.jussieu.fr

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.

Key words: long-term potentiation; long-term depression; dopamine; prefrontal cortex; priming; NMDA receptor

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Received Dec. 13, 2005; revised March 25, 2006; accepted March 25, 2006.

Correspondence should be addressed to Satoru Otani at the above address. Email: satoru.otani{at}snv.jussieu.fr

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