Fieblinger, T., Graves, S. M., Sebel, L. E., Alcacer, C., Plotkin, J. L., Gertler, T. S., … Surmeier, D. J.
Basal Ganglia Pathophysiology Unit, Department Experimental Medical Sciences, Lund University, Lund 22184, Sweden. Department of Physiology, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USA. Picower Institute of Learning and Memory, Massachusetts Institute of Technology, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02139, USA. Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, New York 10065, USA.
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.
… “using a blue LED (full-field stimulation) to excite all cortical afferents (CoolLED, Yorktown Heights, NY)”…
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