| Project/Area Number |
15591229
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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 | Kochi University |
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Principal Investigator |
KATO Kunio Kochi University, Dept.of Neuropsychiatry, Associate Professor, 医学部, 助教授 (70346708)
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| Co-Investigator(Kenkyū-buntansha) |
KODA Kazuhisa Keio University, Physiology, Assistant Professor, 医学部, 講師 (40334388)
SHIMODERA Shinji Kochi University, Neuropsychiatry, Assistant Professor, 医学部附属病院, 講師 (20315005)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | complexin / gene-knockout mouse / maternal deprivation stress / synaptic plasticity / schizophrenia / long-term potentiation / water maze test / hippocampus / complexin / ストレス / 行動学習 / 空間学習 / 長期増強 / stress / schizophernia / animal model / synaptic plasticity / behavior / knockout mouse / PLA2 |
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| Research Abstract |
Complexin II has been reported to be decreased in the brain of schizophrenic patient according to the postmortem study., therefore complexin II could be assumed as the one of actors which contributes the onset of schizophrenia. We investigated the physiological characters of complexin II gene deficient mouse and its vulnerability to the maternal deprivation stress. As a stress model, we adopted the maternal deprivation stress in which the pups were separated from their mother between 2 and 16 day after birth fur one hour every day. We examined the physiological property and behavior of stressed mice. Field excitatory postsynaptic potential was measured with electrophysiological technique in the CA1 area of mouse hippocampus using brain slice preparation. Their spatial memory was examined by Morris Water maze test. The results are summarized as the following. The knockout mouse did not show any particular phenotype. The wild-type mice that were bred under the stressed circumstance also
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did not show abnormality. On the other hand, the knockout mouse that was exposed to the maternal deprivation stress showed the abnormality as the followings. (1)The basic transmission was not differed from that of wild-type mouse. (2)Post-tetanic potentiation, one of the short-term plasticity, which was induced by high frequency electrical stimulation, was significantly decreased in the knockout mouse. (3)The representative synaptic plasticity in the CNS, long-term potentiation, was eliminated in the stressed knockout mouse, whereas long-term depression was not altered. (4)The spatial memory was partially suppressed in the stressed knockout mouse. (5)There was no abnormality in the potential of motor leaning in the stressed mouse.
We concluded that (1)complexin II knockout mouse did not show abnormality in their morphological character and their physiological properties. (2)The maternal deprivation stress affected the brain function in which hippocampus plays a critical role, such as synaptic plasticity and spatial memory, of knockout mouse, whereas, not of the wild-type mouse. (3)The motor learning, in which the cerebellum plays an important role, was not affected. Our results suggest that the complexin II knockout mouse reveals vulnerability during their development to the maternal deprivation stress. Less
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