| Project/Area Number |
07680829
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
TANAKA Jun-ichi Jikei Univ.Sch.of Med., Neuropathol., Professor, 医学部, 教授 (60079712)
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| Co-Investigator(Kenkyū-buntansha) |
MAKIOKA Asao Jikei Univ.Sch.of Med., Tropical Med., Lecturer, 医学部, 講師 (90119850)
WATABE Kazuhiko Tokyo Metropolitan Inst.for Neurosci., Researcher, 研究員 (30240477)
MINAMITANI Motoyuki Jikei Univ.Sch.of Med., Pediatrics, Assistant, 医学部, 助手 (00229775)
FUKUDA Takahiro Jikei Univ.Sch.of Med., Neuropathol., Lecturer, 医学部, 講師 (60228913)
MATSUSHIMA Hiroshi Jikei Univ.Sch.of Med., Pediatrics, Lecturer, 医学部, 講師 (70190460)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1997: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | toxoplasma / intra-uterine infection / mouse / fetal brain / cerebral cortical hypoplasia / apoptosis / TUNEL method / 胎生期感染 / 皮質低形成 / DNA断片 |
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| Research Abstract |
One of the developing disorders in the fetal brain with toxoplasma infection is cortical hypoplasia to which apoptosis may contribute in its process. Congenital toxoplasmosis was induced by intra-peritoneal injection of Toxoplasma gondii (ME49 strain) to the pregnant mice (C57BL/6CrSlc) on gestational day 5 (E5). On E10, E12, E14, E16 and E18 apoptotic cells were demonstrated in the cerebral layrs in both infected and control groups using an in situ end-labeling (TUNEL) method. The cerebral cortex in the infected mice was thinner than in the controls and disclosed an immature laminar architecture. Apoptotic cells distributed mainly in the subependymal layr and occasionally in the intermediate zone. Numbers of the apoptotic cell were counted in the frontal lobes. The cell counts in the control group were 1.67(]SY.+-。[)1.00 (n=9) on E10,1.88(]SY.+-。[)0.99 (n=8) on E12,1.83(]SY.+-。[)1.17(n=6) on E14,1.44(]SY.+-。[)1.75(n=16) on E 16 and 1.56(]SY.+-。[)1.32(n=16) on E18, and in the infected group 3.63(]SY.+-。[)3.70(n=8), 3.50(]SY.+-。[)1.76 (n=6), 3.08(]SY.+-。[)2.11(n=12), 2.18(]SY.+-。[)2.40(n=11) and 1.00(]SY.+-。[)1.71(n=16), respectively. There were considerable differences among individual mice in both groups and statistically a low significance except on E12 (p<0.05). In conclusion an increased number of apoptotic cells in the infected brians could be preceded to that in the controls. This evedence suggests that cell damage might be resulted by a direct protozoal affection to in the fetal brain or by an ischemic influence from placentitis of the infected mother and, therefore, cortical hypoplasia would be induced.
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