2002 Fiscal Year Final Research Report Summary
Neurogenesis and aberrant neuronal reorganization in the hippocampus of the animal models of epilepsy
| Project/Area Number |
13670984
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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 | The University of Tokyo |
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Principal Investigator |
KATO Nobumasa The University of Tokyo, Faculty of Neuropsychiatry, Professor, 医学部附属病院, 教授 (10106213)
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| Co-Investigator(Kenkyū-buntansha) |
MASUI Akira Shiga University of Medical Science, Department of Psychiatry, Lecturer, 医学部, 講師 (80190346)
SADAMATSU Miyuki Health Service Center, Lecturer, 保健センター, 講師 (90252387)
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| Project Period (FY) |
2001 – 2002
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| Keywords | neurogenesis / neuronal cell death / hippocampus / epilepsy / trimethyltin / Noda epileptic rat / glucocorticoid / neuropeptides |
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| Research Abstract |
We investigated the changes in hippocampal neurogenesis after the epileptic seizures using several models of epilepsy ; trimethyltin (TMT)-induced seizure model and spontaneous epileptic strain (Noda epileptic rat : NER). After TMT administration, neurogenesis was significantly decreased in the dentate gyrus at 5-7 d after treatment, and subsequently returned to basal level at 14-28 d. In comparison, the number of newly generated neurons was significantly decreased in the hippocampus of young (7W) NERs compared with their controls, while no significant differences in immunostaining of neurogenic markers were observed between adult (12W) NERs and their controls. Further, we evaluated the effect of neuropeptides and neural immune system on neurogenesis in these models. TMT-administered rats were treated with metyrapone in order to transiently suppress circulating corticosterone. The pathologically low levels of corticosterone induced by metyrapone did not alter the hippocampal damage of TMT at 3-5 d after treatment, however, subsequently increased hippocampal neurogenesis at 14 d after TMT administration. NPY-immunoreactivity increased at 4 d after TMT treatment in the hilus, and progressively decreased to a level below controls at 16 d after treatment. NPY mRNA signals increased in the hilus for 2 days after TMT treatment. In NER, NPY immunoreactivity in the dentate gyrus was continuously elevated, while NPY mRNA increased transiently (within 24 h) after a seizure. These results suggest that both neural immune system and neuropeptides may play a crucial role for the control of neurogenesis after epileptic seizures with different pathogenesis.
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