Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat

Hyoung Chun Kim, Guoying Bing, Wang K. Jhoo, Kwang H. Ko, Won-Ki Kim, Jeong H. Suh, Seong J. Kim, Kanefusa Kato, Jau Shyong Hong

Research output: Contribution to journalArticle

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Abstract

In order to evaluate the putative role of Cu,Zn-superoxide dismutase (SOD-1) in the antioxidant defense mechanism during the neurodegenerative process, we examined the level of mRNA, the specific activity and immunocytochemical distribution for SOD-1 in the rat hippocampus after systemic injection of kainic acid (KA). Hippocampal SOD-1 mRNA levels were significantly increased by the seizure intensity 3 and 7 days after KA. These enhanced mRNA levels for SOD-1 were consistent with the increased specific activities for SOD-1, suggesting that the superoxide radical generated in neurotoxic lesion, induced SOD-1 mRNA. The CA1 and CA3 neurons lost their SOD-1-like immunoreactivity, whereas SOD-1-positive glia-like cells mainly proliferated throughout the CA1 sector and had an intense immunoreactivity at 3 and 7 days after KA. This immunocytochemical distribution for SOD-1-positive non-neuronal elements was similar to that for glial fibrillary acidic protein (GFAP)-positive cells. Each immunoreactivity for SOD-1-positive non-neuronal cell or GFAP in the layers of CA1 and CA3 disappeared 3 and 7 days after a maximal stage 5 seizure. On the other hand, activated microglial cells as selectively marked with the lectin occurred in the areas affected by KA-induced lesion. Double-labeling immunocytochemical analysis demonstrated the co-localization of SOD-1-positive glia-like cells and reactive astrocytes as labeled by GFAP or S-100 protein immunoreactivity. This finding suggested that the mobilization of astroglial cells for the synthesis of SOD-1 protein is a response to the KA insult designed to decrease the neurotoxicity induced by oxygen-derived free radicals. Therefore, these alterations might reflect the regulatory role of SOD-1 against oxygen-derived free radical-induced neuronal degeneration after systemic KA administration. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)215-226
Number of pages12
JournalBrain Research
Volume853
Issue number2
DOIs
Publication statusPublished - 2000 Jan 24
Externally publishedYes

Fingerprint

Kainic Acid
Glial Fibrillary Acidic Protein
Messenger RNA
Neuroglia
Free Radicals
Seizures
Therapeutics
Oxygen
S100 Proteins
Protein S
Lectins
Superoxides
Astrocytes
Superoxide Dismutase-1
Hippocampus
Antioxidants
Neurons
Injections

Keywords

  • Astrocyte
  • Cu,Zn-superoxide dismutase
  • Free radical
  • Hippocampus
  • Kainic acid
  • Microglia
  • Neurodegeneration
  • Superoxide

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Kim, H. C., Bing, G., Jhoo, W. K., Ko, K. H., Kim, W-K., Suh, J. H., ... Hong, J. S. (2000). Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat. Brain Research, 853(2), 215-226. https://doi.org/10.1016/S0006-8993(99)02254-4

Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat. / Kim, Hyoung Chun; Bing, Guoying; Jhoo, Wang K.; Ko, Kwang H.; Kim, Won-Ki; Suh, Jeong H.; Kim, Seong J.; Kato, Kanefusa; Hong, Jau Shyong.

In: Brain Research, Vol. 853, No. 2, 24.01.2000, p. 215-226.

Research output: Contribution to journalArticle

Kim, HC, Bing, G, Jhoo, WK, Ko, KH, Kim, W-K, Suh, JH, Kim, SJ, Kato, K & Hong, JS 2000, 'Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat', Brain Research, vol. 853, no. 2, pp. 215-226. https://doi.org/10.1016/S0006-8993(99)02254-4
Kim, Hyoung Chun ; Bing, Guoying ; Jhoo, Wang K. ; Ko, Kwang H. ; Kim, Won-Ki ; Suh, Jeong H. ; Kim, Seong J. ; Kato, Kanefusa ; Hong, Jau Shyong. / Changes of hippocampal Cu/Zn-superoxide dismutase after kainate treatment in the rat. In: Brain Research. 2000 ; Vol. 853, No. 2. pp. 215-226.
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