2005 Fiscal Year Final Research Report Summary
Developmental expression of the Wolfram syndrome gene in the mouse brain
| Project/Area Number |
15591228
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Kagoshima University (2005)
Yamaguchi University (2003-2004) |
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Principal Investigator |
KAWANO June Kagoshima University, Graduate School of Medical and Dental Sciences, Research Associate, 大学院・医歯学総合研究科, 助手 (80251924)
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| Co-Investigator(Kenkyū-buntansha) |
SHINODA Koh Yamaguchi University, School of Medicine, Professor, 医学部, 教授 (40192108)
YANAI Akie Yamaguchi University, School of Medicine, Research Associate, 医学部, 助手 (20284854)
FUJINAGA Ryutaro Yamaguchi University, School of Medicine, Research Associate, 医学部, 助手 (30335723)
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| Project Period (FY) |
2003 – 2005
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| Keywords | Wolfram syndrome / neurodegenerative disorder / gene expression / Wfs1 / brain / mouse / postnatal development / histochemistry |
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| Research Abstract |
Mutations of the WFS1 gene are responsible for Wolfram syndrome (WS), an autosomal recessive neurodegenerative disorder. There is evidence suggesting that subjects affected with WS present an increased risk of psychiatric disorders, particularly depression and suicidal behavior. To obtain neuroanatomical evidence for understanding the psychiatric pathophysiology of WS as well as WFS1 protein function, we investigated postnatal development of Wfs1 expression in the male mouse brain by using histochemical methods.
Wfs1 mRNA expression was classified into three types according to temporal pattern of development. In type 1 expression, Wfs1 mRNA signals were weak on delivery day (P0), progressively increased from PO to postnatal day 14 (P14), and showed relatively stable strength from P14 to the young adult stage. The signals were seen in the limbic cortex (hippocampal CA1 etc.). In type 2 expression, Wfs1 mRNA signals showed relatively constant strength during the postnatal development. The signals were observed in the limbic structures (central amygdaloid nucleus etc.), and in the brainstem motor nuclei (facial nucleus etc.). In type 3 expression, Wfs1 mRNA signals peaked at P7-P14, and were seen in the thalamic reticular nucleus. In considerable number of limbic structures, Wfs1 mRNA signals represented moderate-to-strong strength from P7 to the young adult stage. Results obtained suggest that Wfs1 plays an important role during limbic system development and that Wfs1 is responsible for the maintenance of limbic system function. The results also suggest that the limbic system in WS patients might be affected by WFS1 mutations from birth to adulthood. Neuroanatomical investigation of Wfs1 mutant mice will be required in the next step.
In addition, we studied Wfs1 expression in the mouse pancreatic islet and retina, sex steroid hormone receptor expression in the rat and mouse dorsal raphe nuclei, and Hap1 mRNA expression in the mouse brain.
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Research Products
(6 results)
