1998 Fiscal Year Final Research Report Summary
A study of transgenic mice with reduced calbindin-D28K expression
| Project/Area Number |
08671108
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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 | Juntendo University |
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Principal Investigator |
TAKAHASHI Tadashi Juntendo University School of Medicine, Assistant, 医学部, 助手 (30236294)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Hajime Juntendo University School of Medicine, Assistant, 医学部, 助手
OHNUMA Tohru Juntendo University School of Medicine, Assistant, 医学部, 助手 (10286734)
NISHIYAMA Etsuko Juntendo University School of Medicine, Assistant, 医学部, 助手 (70286748)
IWAMOTO Norihiko Juntendo University School of Medicine,, 医学部, 講師 (60211067)
ARAI Heii Juntendo University School of Medicine, Profesor, 医学部, 教授 (50167988)
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| Project Period (FY) |
1996 – 1998
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| Keywords | calcium binding protein / calbindin / transgenic mice / antisense RNA / in situ hybridization / immunohistochemistry / Alzheimer-type dementia / parvalbumin |
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| Research Abstract |
In situ hybridization and immunohistochemical studies showed that this antisense construct abolishes calbindin (GB) mRNA and protein expression in the forebrain and midbrain of the transgenic (Tg) mice in a dose dependent manner. It is interesting to .note that the sense hybridiza-tion signal was dramatically reduced in cerebellar Purkinje cells (approximately -10%) which express the highest levels of GB mRNA and protein. Other histochemical and quantitative analysis (HE, Nissi, Holzer and KB stain) of old mice(postnatal 24 months) tissue sections indicated that there were no gross abnormalities or cell loss in any of the forebrain structures. On the other hand, learning and memory capacities have been assesed. Homozygous mice were significantly worse at reaching an asymptote of working level performance than control mice. We have also indicated that a dramatic decrease in hippocampal (CAl) long-term potentiation in the Tg mice. These Tg mice may be valuable in the study of learning and memory mechanism including some of ATD pathology.
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