Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia

Tim Fieblinger, Steven M. Graves, Luke E. Sebel, Cristina Alcacer, Joshua L. Plotkin, Tracy S. Gertler, C. Savio Chan, Myriam Heiman, Paul Greengard, M. Angela Cenci and D. James Surmeier ()
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Tim Fieblinger: Basal Ganglia Pathophysiology Unit, Lund University
Steven M. Graves: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA
Luke E. Sebel: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA
Cristina Alcacer: Basal Ganglia Pathophysiology Unit, Lund University
Joshua L. Plotkin: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA
Tracy S. Gertler: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA
C. Savio Chan: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA
Myriam Heiman: Picower Institute of Learning and Memory, Massachusetts Institute of Technology, Broad Institute of MIT and Harvard
Paul Greengard: Laboratory of Molecular and Cellular Neuroscience, Rockefeller University
M. Angela Cenci: Basal Ganglia Pathophysiology Unit, Lund University
D. James Surmeier: Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA

Nature Communications, 2014, vol. 5, issue 1, 1-15

Abstract: Abstract The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson’s disease (PD) and L-DOPA-induced dyskinesia (LID). In these disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is disrupted, leading to aberrant action selection. However, it is unclear whether countervailing mechanisms are engaged in these states. Here we report that iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD models than normal; L-DOPA treatment restored these properties. Conversely, dSPN intrinsic excitability was elevated in tissue from PD models and suppressed in LID models. Although the synaptic connectivity of dSPNs did not change in PD models, it fell with L-DOPA treatment. In neither case, however, was the strength of corticostriatal connections globally scaled. Thus, SPNs manifested homeostatic adaptations in intrinsic excitability and in the number but not strength of excitatory corticostriatal synapses.

Date: 2014
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DOI: 10.1038/ncomms6316

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