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Basic mechanisms of seizure susceptibility and seizure induction in kindling model of epilepsy. Mitsumoto SATO 1 , Kiyoshi MORIMOTO 2 1Department of Neuropsychiatry, Tohoku University Medical School 2Department of Neuropsychiatry, Okayama University Medical School pp.884-891
Published Date 1989/12/10
DOI https://doi.org/10.11477/mf.1431906340
  • Abstract
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We reviewed here neuronal changes in excitatory amino acid-mediated transmission in the kindling model of epilepsy which results from repeated focal electrical stimulation. First, we suggested that kindled permanent epileptogenesis could be developed via repeated activation of N-methyl-D-aspartate (NMDA) receptors. Second, it was indicated that lasting increase in non-NMDA receptor mediated polyphosphoinositide hydrolysis might be important in long-lasting seizure susceptibility of kindling. Finally, in seizure-triggering mechanisms of kindling, we concluded that the secondary relative weakness (disinhibition) of inhibitory systems, e.g. GABA and/or TRH systems, might be more important than the primary excitation of excitatory amino acid systems. (Received: June 15, 1989)


Copyright © 1989, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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