Experimental study on functional pathology of dystonia

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430054
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: The University of Tokushima
• Principal Investigator: GOTO Satoshi 徳島大学, 大学院医歯薬学研究部(医学系), 特任教授 (50240916)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 神経変性疾患 / ジストニア / 神経病理 / 線条体 / ストリオソーム / マトリックス / ドパミン

Outline of Final Research Achievements

In the mammalian striatum that plays a central role in the basal ganglia circuit, there exist two functional subdivisions known as striosome and matrix compartments. During the last 3 years, we found a selective loss of dopamine D1 receptor (D1R)-mediated signals in the striosome compartment in transgenic mouse and human disease models with dystonia. Moreover, we provided the evidence that striatal neurodegeneration causing dystonia might be associated with a lack of striosomal expression of neuroprotective molecules that include neuropeptide Y and postsynaptic density protein 95 (PSD-95). These findings corroborate with the hypothesis that deregulation of D1 signaling in the striosome compartment may underlie the genesis of dystonia.

Free Research Field

臨床神経科学