| Project/Area Number |
06680790
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neuroscience in general
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| Research Institution | Osaka City University |
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Principal Investigator |
MATSUURA Shiushi Osaka City University Medical School, Department of PHysiology, Professor, 医学部, 教授 (50047007)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Augmentation / Amygdala kindling / Entorhinal cortex / Facilitation / hippocampus / NMDA receptor antagonist / GABA receptor / Excitatory synaptic transmission / 嗅内野誘発反応 / 促進現象 / 長期増強作用 / NMDA受容体 / CPP |
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| Research Abstract |
Entorhinal posttetanic responses (PTRs) to 10 single (0.3Hz) stimuli immediately after train stimulus (10Hz, 100 pulses) to the amygdala were recorded from conscious rats, which had electrodes previously implanted under pentobarbital anesthesia, and the magnitude of PTRs was estimated as the area between the negative potential ascribable to excitatory activation in the averaged PTR and the baseline. When the stimulus intensity was 50-100 mA lower than threshold to induce afterdischarges (ADs), the averaged PTR showed the same magnitude as the averaged test response before train, showing no augmentation in the PTR.However, augmentation in the PTR was apparent at the intensity 25 mA lower than the AD threshold and progressively increased untill the intensity became the AD threshold. The magnitude of the averaged PTR (except for some 1-3 PTRs superimposed on ADs) was more markedly increased and showed a linear relation to the AD duration, when train stimulus with the AD threshold intensity was repeated untill the AD duration became about 30 s. The increase of PTR first occurred in the mono- and later in the polysynaptic component during the developmental stages of kindling. In the hippocampal PTRs, augmentation became to be increased more latoly than in the entorhinal cortex. An NMDA receptor antagonist (CPP) and GABA receptor agonist (pentobarbital) markedly deppressed ADs and blocked kindling seizures in association with a decrease in augmentation in PTRs. These results indicate that enhancement of augmentation based on NMDA receptor activation in the PTR is involved in the origin of development of ADs and seizures during the early course of kindling.
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