English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

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

MPS-Authors
There are no MPG-Authors available
Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Matsuda, Y., Marzo, A., & Otani, S. (2006). The Presence of Background Dopamine Signal Converts Long-Term Synaptic Depression to Potentiation in Rat Prefrontal Cortex. The 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.