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Cerebral Cortex Advance Access originally published online on March 12, 2009
Cerebral Cortex 2009 19(11):2708-2718; doi:10.1093/cercor/bhp047
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Background Dopamine Concentration Dependently Facilitates Long-term Potentiation in Rat Prefrontal Cortex through Postsynaptic Activation of Extracellular Signal-Regulated Kinases

B. Kolomiets1,4, A. Marzo1,5, J. Caboche2,5, P. Vanhoutte2,5 and S. Otani1,3,5

1 Laboratory of Neuromodulation, Neuronal Plasticity and Cognition, 2 Laboratory of Neuronal Signalisation and Genetic Regulation, CNRS-UMR7102, Université Paris VI Pierre et Marie Curie, Paris, France, 3 Sophia University Open Research Centre, Tokyo, Japan, 4 Current address: Cellular and Molecular Physiopathology of Retina, INSERM U-592, Paris, France, 5 Current address: Physiopathology of Central Nervous System Diseases, INSERM U-952/CNRS-UMR7224, Universié Paris VI Pierre et Marie Curie, Paris, France

Address correspondence to Satoru Otani, University of Paris VI Pierre and Marie Curie, Building B, 6th floor, Room 620, 7 quai St Bernard, 75005 Paris, France. Email: satoru.otani{at}snv.jussieu.fr.

Altered levels of tonic/background dopamine in prefrontal cortex (PFC) may underlie modifications of executive cognitive function. We showed previously in rat PFC slices that exogenously supplied background dopamine facilitates induction of long-term potentiation (LTP), a possible cellular substrate for the long-term component of executive cognitive function. In the present study, we characterized cellular and molecular mechanisms underlying this modulatory dopamine effect. We show first that the LTP-facilitating effect of tonic/background dopamine follows an inverted-U shape concentration curve and that the effective level of background dopamine slowly activates postsynaptic extracellular signal-regulated kinases (ERKs) to facilitate LTP. Furthermore, we show the evidence that LTP-inducing high-frequency stimulation evokes endogenous release of dopamine in PFC slices. This fast dopamine serves as a trigger for LTP in the presence of the background dopamine. In its absence, the endogenous dopamine triggered, instead, long-term depression. These results indicate that appropriate levels of tonic/background dopamine serve to activate critical molecular factors in PFC neurons and thereby facilitate induction of synaptic potentiation.

Key Words: dopamine • ERK • LTD • LTP • prefrontal cortex


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