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The Journal of Neuroscience, March 5, 2008, 28(10):2435-2446; doi:10.1523/JNEUROSCI.4402-07.2008
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Cellular/Molecular
Dopamine Receptor Activation Is Required for Corticostriatal Spike-Timing-Dependent Plasticity
Verena Pawlak1,2 andJason N. D. Kerr2 1Department of Cell Physiology, Max Planck Institute for Medical Research, 69120 Heidelberg, Germany, and 2Network Imaging Group, Max Planck Institute for Biological Cybernetics, 72076 Tübingen, Germany
Correspondence should be addressed to either Verena Pawlak or Jason N. D. Kerr, Network Imaging Group, Max Planck Institute for Biological Cybernetics, Spemannstrasse 41, 72076 Tübingen, Germany, Email: verena.pawlak{at}tuebingen.mpg.de or Email: jason{at}tuebingen.mpg.de
Single action potentials (APs) backpropagate into the higher-order dendrites of striatal spiny projection neurons during cortically driven "up" states. The timing of these backpropagating APs relative to the arriving corticostriatal excitatory inputs determines changes in dendritic calcium concentration. The question arises to whether this spike-timing relative to cortical excitatory inputs can also induce synaptic plasticity at corticostriatal synapses. Here we show that timing of single postsynaptic APs relative to the cortically evoked EPSP determines both the direction and the strength of synaptic plasticity in spiny projection neurons. Single APs occurring 30 ms before the cortically evoked EPSP induced long-term depression (LTD), whereas APs occurring 10 ms after the EPSP induced long-term potentiation (LTP). The amount of plasticity decreased as the time between the APs and EPSPs was increased, with the resulting spike-timing window being broader for LTD than for LTP. In addition, we show that dopamine receptor activation is required for this spike-timing-dependent plasticity (STDP). Blocking dopamine D1/D5 receptors prevented both LTD and LTP induction. In contrast, blocking dopamine D2 receptors delayed, but did not prevent, LTD and sped induction of LTP. We conclude (1) that, in combination with cortical inputs, single APs evoked in spiny projection neurons can induce both LTP and LTD of the corticostriatal pathway; (2) that the strength and direction of these synaptic changes depend deterministically on the AP timing relative to the arriving cortical inputs; (3) that, whereas dopamine D2 receptor activation modulates the initial phase of striatal STDP, dopamine D1/D5 receptor activation is critically required for striatal STDP. Thus, the timing of APs relative to cortical inputs alone is not enough to induce corticostriatal plasticity, implying that ongoing activity does not affect synaptic strength unless dopamine receptors are activated.
Key words: striatum; basal ganglia; NMDA receptors; spiny projection neuron; synaptic plasticity; excitatory synaptic transmission
Received Sept. 26, 2007; revised Dec. 14, 2007; accepted Jan. 9, 2008.
Correspondence should be addressed to either Verena Pawlak or Jason N. D. Kerr, Network Imaging Group, Max Planck Institute for Biological Cybernetics, Spemannstrasse 41, 72076 Tübingen, Germany, Email: verena.pawlak{at}tuebingen.mpg.de or Email: jason{at}tuebingen.mpg.de
This article has been cited by other articles:
W. Shen, M. Flajolet, P. Greengard, and D. J. Surmeier
Dichotomous Dopaminergic Control of Striatal Synaptic Plasticity
Science, August 8, 2008; 321(5890): 848 - 851.
[Abstract] [Full Text] [PDF]
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