1996年11月
Characterization of epileptiform field potentials recorded in the in vitro perirhinal cortex of amygdala-kindled epileptogenesis
BRAIN RESEARCH
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- 巻
- 741
- 号
- 1-2
- 開始ページ
- 44
- 終了ページ
- 51
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/S0006-8993(96)00878-5
- 出版者・発行元
- ELSEVIER SCIENCE BV
The perirhinal cortex (PRC) has recently been reported that the excitatory role of this area is important for the generation and the propagation of kindled seizures. In the present study, we investigated the extracellular electrophysiological properties of the circuitry which contribute to the propagation of seizures in the PRC, and examined the hypothesis that amygdala-kindling changes the electrophysiological nature of the rat PRC slice in vitro. Field potentials elicited in the PRC had extended duration (> 200 ms, most congruent to 1 s) with overlying spike components. The potentials showed strong synchronizing effect governed by an all-or-none rule. Although spontaneous epileptiform discharges that were equivalent in appearance to synaptically-activated field potentials were observed in the PRC of both amygdala-kindled and control rats, the number of slices showing spontaneous activity was significantly larger in the kindled group than in the control group (chi(2)-test, P < 0.01). The occurrence of tetanus-induced afterdischarges in kindled rats was significantly higher than in control rats (chi(2)-test, P < 0.01). The afterdischarge durations of control slices were generally short and the afterdischarges did not consist of the typical 'tonic-clonic' phases. However, the occurrence of the electrographical seizure in the high K+ ACSF were not affected by amygdala-kindling operation. These results indicate that amygdala-kindling lowers the threshold for transsynaptic excitability and enhances the synchronized activity of the PRC induced by episodic proconvulsive manipulations such as tetanus stimulation.
- リンク情報
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- DOI
- https://doi.org/10.1016/S0006-8993(96)00878-5
- CiNii Articles
- http://ci.nii.ac.jp/naid/30003066583
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/9001703
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:A1996VZ08100006&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1016/S0006-8993(96)00878-5
- ISSN : 0006-8993
- CiNii Articles ID : 30003066583
- PubMed ID : 9001703
- Web of Science ID : WOS:A1996VZ08100006