An experimental study on the course of trans-synaptic propagation of neural activity and plasticity in the hippocampus in kainate-induced epilepsy

Keiko Sato, Koji Abe

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

To investigate the course of trans-synaptic propagation of neural activity and plasticity in temporal lobe epilepsy, time-dependent changes in the level of synapsin I, a synaptic vesicle protein that is a marker of enhanced synaptic activity and synaptogenesis, were examined following kainate-induced epileptic status in rats. Compared with the control, the level of synapsin I protein increased in the bilateral stratum oriens of CA3 (28.8-40.2%) and CA1 (28.0-34.6%), and the stratum radiatum of CA1 (34.0%) ipsilateral to the injection site at 8 h after intra-amygdala administration of kainate. At 24 h, and 2 and 4 weeks after the kainate treatment, however, synapsin I levels returned to normal levels in most of the regions studied in spite of the extended neural loss in the hippocampus, which suggested the axonal sprouting on the remaining cells. The synapsin I mRNA levels time-dependently decreased bilaterally in CA1-CA3 and the hilus, while no significant changes were observed in the dentate gyrus. These results suggest that the synaptic input to CA3 and CA1 through the stratum oriens was enhanced in this model. A different mode of hippocampal neural activity and plasticity between kainate and kindling models of epilepsy may be stressed.

Original languageEnglish
Pages (from-to)393-400
Number of pages8
JournalBrain Research Bulletin
Volume55
Issue number3
DOIs
Publication statusPublished - 2001

Fingerprint

Synapsins
Neuronal Plasticity
Kainic Acid
Epilepsy
Hippocampus
Hippocampal CA1 Region
Temporal Lobe Epilepsy
Synaptic Vesicles
Dentate Gyrus
Amygdala
Proteins
Messenger RNA
Injections

Keywords

  • Epileptic status
  • Hippocampus
  • Immunohistochemistry
  • In situ hybridization
  • Kainic acid
  • Synapsin I

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "An experimental study on the course of trans-synaptic propagation of neural activity and plasticity in the hippocampus in kainate-induced epilepsy",
abstract = "To investigate the course of trans-synaptic propagation of neural activity and plasticity in temporal lobe epilepsy, time-dependent changes in the level of synapsin I, a synaptic vesicle protein that is a marker of enhanced synaptic activity and synaptogenesis, were examined following kainate-induced epileptic status in rats. Compared with the control, the level of synapsin I protein increased in the bilateral stratum oriens of CA3 (28.8-40.2{\%}) and CA1 (28.0-34.6{\%}), and the stratum radiatum of CA1 (34.0{\%}) ipsilateral to the injection site at 8 h after intra-amygdala administration of kainate. At 24 h, and 2 and 4 weeks after the kainate treatment, however, synapsin I levels returned to normal levels in most of the regions studied in spite of the extended neural loss in the hippocampus, which suggested the axonal sprouting on the remaining cells. The synapsin I mRNA levels time-dependently decreased bilaterally in CA1-CA3 and the hilus, while no significant changes were observed in the dentate gyrus. These results suggest that the synaptic input to CA3 and CA1 through the stratum oriens was enhanced in this model. A different mode of hippocampal neural activity and plasticity between kainate and kindling models of epilepsy may be stressed.",
keywords = "Epileptic status, Hippocampus, Immunohistochemistry, In situ hybridization, Kainic acid, Synapsin I",
author = "Keiko Sato and Koji Abe",
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T1 - An experimental study on the course of trans-synaptic propagation of neural activity and plasticity in the hippocampus in kainate-induced epilepsy

AU - Sato, Keiko

AU - Abe, Koji

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N2 - To investigate the course of trans-synaptic propagation of neural activity and plasticity in temporal lobe epilepsy, time-dependent changes in the level of synapsin I, a synaptic vesicle protein that is a marker of enhanced synaptic activity and synaptogenesis, were examined following kainate-induced epileptic status in rats. Compared with the control, the level of synapsin I protein increased in the bilateral stratum oriens of CA3 (28.8-40.2%) and CA1 (28.0-34.6%), and the stratum radiatum of CA1 (34.0%) ipsilateral to the injection site at 8 h after intra-amygdala administration of kainate. At 24 h, and 2 and 4 weeks after the kainate treatment, however, synapsin I levels returned to normal levels in most of the regions studied in spite of the extended neural loss in the hippocampus, which suggested the axonal sprouting on the remaining cells. The synapsin I mRNA levels time-dependently decreased bilaterally in CA1-CA3 and the hilus, while no significant changes were observed in the dentate gyrus. These results suggest that the synaptic input to CA3 and CA1 through the stratum oriens was enhanced in this model. A different mode of hippocampal neural activity and plasticity between kainate and kindling models of epilepsy may be stressed.

AB - To investigate the course of trans-synaptic propagation of neural activity and plasticity in temporal lobe epilepsy, time-dependent changes in the level of synapsin I, a synaptic vesicle protein that is a marker of enhanced synaptic activity and synaptogenesis, were examined following kainate-induced epileptic status in rats. Compared with the control, the level of synapsin I protein increased in the bilateral stratum oriens of CA3 (28.8-40.2%) and CA1 (28.0-34.6%), and the stratum radiatum of CA1 (34.0%) ipsilateral to the injection site at 8 h after intra-amygdala administration of kainate. At 24 h, and 2 and 4 weeks after the kainate treatment, however, synapsin I levels returned to normal levels in most of the regions studied in spite of the extended neural loss in the hippocampus, which suggested the axonal sprouting on the remaining cells. The synapsin I mRNA levels time-dependently decreased bilaterally in CA1-CA3 and the hilus, while no significant changes were observed in the dentate gyrus. These results suggest that the synaptic input to CA3 and CA1 through the stratum oriens was enhanced in this model. A different mode of hippocampal neural activity and plasticity between kainate and kindling models of epilepsy may be stressed.

KW - Epileptic status

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KW - Immunohistochemistry

KW - In situ hybridization

KW - Kainic acid

KW - Synapsin I

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