Contribution of neuronal regeneration in the hippocampus and dentate gyrus to the memory disturbance after traumatic brain injury
| Project/Area Number |
17500279
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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 |
Neurophysiology and muscle physiology
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| Research Institution | Kurume University |
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Principal Investigator |
AKASU Takashi Kurume University, School of Medicine, Professor, 医学部, 教授 (60113213)
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| Co-Investigator(Kenkyū-buntansha) |
HASUO Hiroshi Kurume University, School of Medicine, Associate Professor, 医学部, 助教授 (90172882)
TAKEYA Mitsue Kurume University, School of Medicine, Assistant Professor, 医学部, 助手 (30289433)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2006: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2005: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | brain injury / dentate gyrus / hippocampal CA1 / glutamate neurons / diazepam / NO scavengers / epilepsy / memory disturbance / 頭部外傷モデル / 興奮性シナプス伝達 / グルタミン酸 / ガンマーアミノ酪酸 |
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| Research Abstract |
Animal model of experimental brain injury was made by application of moderate fluid percussion injury (FPI) to the left parietal cortex of rat brain. Horizontal brain slices of hippocampal CA1 area and dentate gyrus were obtained from FPI rats. Optical responses with voltage-sensitive dye (RH-482) showed that stimulation of the Schaffer collaterals or perforant path evoked the propagation of excitatory optical signals to hippocampal CA1 area or dentate gyrus (DG). Intracellular recordings showed that FPI enhanced the amplitude and duration of excitatory postsynaptic potentials (EPSPs). The EPSP was further enhanced by bicuculline (15 μM) in FPI rat hippocampal neurons. FPI strongly depressed long-term potentiation (LTP) in hippocampal CA1 area. Long-term depression (LTD) was relatively obvious in FPI rats. However, electrophysiological properties of single neurons in the CA1 and the DG were not obviously altered by FPI. No obvious sprouting of glutamate neurons occurred after FPI. Intraperitoneal (i.p.) administration of diazepam (a benzodiazepine derivative) 30-90 min after FPI protected hippocampal CA1 area against the head injury. The NMDA-receptor component of the field EPSP (fEPSP) was selectively depressed by diazepam and edaravone, a nitric oxide scavenger, in FPI rats. Hypothermia (35℃) also attenuated the FPI-induced hyperactivity of hippocampal CA1 neurons. Administration of edaravone at early period (30-90 min) after FPI, prevented the FPI-induced hyperactivity and pathological LTP in hippocampal CA1 neurons.
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Report
(3 results)
Research Products
(89 results)
