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A seizure triggering mechanism of spontaneous epileptiform potential in the hippocampus
http://hdl.handle.net/10458/2165
http://hdl.handle.net/10458/21659f1f36b7-33e0-4077-bfda-6191369ae0d1
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
2-5b(1-13b).pdf (1.4 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2009-08-17 | |||||
| タイトル | ||||||
| タイトル | A seizure triggering mechanism of spontaneous epileptiform potential in the hippocampus | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ | journal article | |||||
| 著者 |
Tsuru, Noriko
× Tsuru, Noriko× Ueda, Yuto |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Kindling is now popular as a model of epilepsy as well as of neuronal plasticity. In this review we explain the neuronal mechanism of the spontaneous epileptiform potential in hippocampi of kindled animals. The epileptogenic properties have been presumed to be a combination of （a） aggregates of hyperexcitable epileptic neurons and （b） a decrease in inhibitory influences. However, the interictal state of epileptogenic focus seemed to be hypoexcitable, as shown by the recent topographical study using PET or SPECT findings. Therefore it is difficult to understand the epileptogenic focus from the view point of hyperexcitability. We reported that although there was an enormous outflow of the extracellular glutamate during kindled seizure in the interictal state, there was no difference compared to baseline. On the other hand, there was a gradual increase of the GABA level even in the interictal state using the microdialysis technique）. These facts suggest to us the inhibitory mechanism of GABA, which increased after the accomplishment of kindling, even 24 hours after seizure. Therefore, as a result of the strengthened inhibitory mechanism in the interictal state, the many pyramidal cells tend to cease firing. However, in the area CA1 there will be a facilitation because of the enormous outflow of glutamate. Because of the increased GABA level in the gate of input, when the bombardment of the impulses to the dentate gyrus occur, almost all of the multitude of resulting resting cells fire at the same time and propagate to CA1. At CA1, on the other hand, the seizure triggering mechanisms start at the point of output, because of the enormous induced outflow of glutamate. | |||||
| 言語 | en | |||||
| 書誌情報 |
en : Journal of brain science ja : 日本脳科学会会誌 巻 23, 号 1, p. 61-78, 発行日 1997 |
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| 出版者 | ||||||
| 出版者 | 日本脳科学会 | |||||
| 言語 | ja | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 13415301 | |||||
| 書誌レコードID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11081225 | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
