| Project/Area Number |
14580793
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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 |
神経・脳内生理学
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
AKASU Takashi Kurume Univ. Sch. Med, Professor, 医学部, 教授 (60113213)
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| Co-Investigator(Kenkyū-buntansha) |
HASUO Hiroshi Kurume Univ. Sch. Med., Associate Prof., 医学部, 助教授 (90172882)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | post-traumatic epilepsy / experimental head injury model rat / hippocampal slice preparation / post-traumatic excitation / long-term potentiation (LTP) / whole-cell patch-clamp recordings / excitatory synaptic transmission / EPSP |
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| Research Abstract |
Horizontal brain slice preparations were obtained from experimental brain injury model rats by application of moderate fluid percussion injury (FPI) to the left parietal cortex of rat brain. Electrical stimulation of hippocampal CA3 pyramidal neurons stained by voltage-sensitive dye (RH-482) evoked the propagation of excitatory optical signals to CA1 pyramidal area. The excitatory optical response was enhanced at injured site (ipsilateral) of hippocampal formation. Field potentials of hippocampal pyramidal layer recorded by extracellular electrode was also enhanced at ipsilateral hippocampal CA1 area. Intracellular recordings revealed that long-term potentiation (LTP) was depressed in FPI rats. LTD was relatively obvious in FPI rats. However, electrophysiological properties of single CA1 neurons were not obviously altered by FPI. Emodin, (an anthraquinone derivative) which protect brain from head injury, depressed the evoked and spontaneous release of glutamate from nerve terminals of the Schaffer collaterals.
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