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ID 116978
Title Alternative
マウス線条体ニューロンにおけるオプチニューリンの細胞特異的局在 : ハンチントン病における神経脆弱性への影響
Author
Koizumi, H. Tokushima University
Keywords
Huntington's disease
optineurin
Huntingtin
medium spiny neuron
Tyramide Signal Amplification
striatum
interneurons
neurodegeneration
Content Type
Thesis or Dissertation
Description
Striatal neuropathology of Huntington's disease (HD) involves primary and progressive degeneration of the medium-sized projection neurons, with relative sparing of the local circuit interneurons. The mechanism for such a patterned cell loss in the HD striatum continues to remain unclear. Optineurin (OPTN) is one of the proteins interacting with huntingtin and plays a protective role in several neurodegenerative disorders. To determine the cellular localization pattern of OPTN in the mouse striatum, we employed a highly sensitive immunohistochemistry with the tyramide signal amplification system. In this study, we show that OPTN appeared as a cytoplasmic protein within the subsets of the striatal neurons. Of particular interest was that OPTN was abundantly expressed in the interneurons, whereas low levels of OPTN were observed in the medium projection neurons. This cell type-specific distribution of OPTN in the striatum is strikingly complementary to the pattern of neuronal loss typically observed in the striatum of patients with HD. We suggest that OPTN abundance is an important cellular factor in considering the cell type-specific vulnerability of striatal neurons in HD.
Journal Title
Neuroscience
ISSN
03064522
NCID
AA0075489X
AA11540865
Publisher
Elsevier|International Brain Research Organization
Volume
202
Start Page
363
End Page
370
Published Date
2011-12-03
Remark
内容要旨・審査要旨・論文本文の公開
本論文は,著者S. Okitaの学位論文として提出され,学位審査・授与の対象となっている。
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
ETD
MEXT report number
甲第3587号
Diploma Number
甲医第1528号
Granted Date
2022-03-16
Degree Name
Doctor of Medical Science
Grantor
Tokushima University
departments
University Hospital
Medical Sciences