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Quarter Century after the Direct and Indirect Pathways: Towards Comprehensive Understandings of the Basal Ganglia

開催日 2014/9/13
時間 9:00 - 11:00
会場 Room B(501)
Chairperson(s) 南部 篤 / Atsushi Nambu (生理学研究所 生体システム研究部門 / Division of System Neurophysiology, National Institute for Physiological Sciences, Japan)
藤山 文乃 / Fumino Fujiyama (同志社大学・脳科学研究科 / Laboratory of Neural Circuitry, Graduate School of Brain Science, Doshisha University, Kyoto, Japan)

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

  • S3-B-1-1
  • Dalton James Surmeier, Jr.:1 
  • 1:Department of Physiology, Northwestern University, Feinberg School of Medicine, USA 

The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson’s disease (PD) and L- DOPA-induced dyskinesia (LID). In these two closely related dopamine-dependent disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is thought to be disrupted, leading to aberrant action selection. This view is based upon the dichotomous dopaminergic modulation of these two pathways through D1 and D2 receptors. However, current models of these states do not account for the propensity of neural circuits to homeostatically correct sustained perturbations in activity. To determine if homeostatic mechanisms were engaged in PD and LID models, SPNs were studied in /ex vivo /brain slices. These studies revealed that SPNs manifested homeostatic adaptations in intrinsic excitability and excitatory corticostriatal connectivity to re-balance average activity in both PD and LID models. However, synaptic strength was not homeostatically scaled in parallel, potentially leading to inappropriately timed and scaled activity. This aberrant activity should be particularly prominent in LID models where both iSPNs and dSPNs undergo substantial synaptic reorganization. Strategies for ameliorating these pathological
adaptations will be discussed.

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