Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment

Hyoung Chun Kim, Guoying Bing, Wang Kee Jhoo, Won-Ki Kim, Eun Joo Shin, Eon Sup Park, Yong Soon Choi, Dong Wook Lee, Chan Young Shin, Jae Ryun Ryu, Kwang Ho Ko

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40 Citations (Scopus)

Abstract

We have demonstrated that seizures induced by kainic acid (KA) are, at least in part, mediated via oxidative stress in rats [Life. Sci. 61 (1997) PL373; Brain Res. 853 (2000) 215; Brain Res. 874 (2000) 15; Neurosci. Lett. 281 (2000) 65]. In order to extend our findings, we employed the rodent aging model in this study. After KA treatments (once a day for 5 days; 20, 20, 20, 20 and 40 mg/kg, i.p.), several parameters reflecting neurotoxic behaviors, oxidative stress [malondialdehyde (MDA) and protein carbonyl] and aging (lipofuscin-like substances) were compared between senile-prone (P8) and resistant (R1) strains of 9-month-old male senescence-accelerated mice (SAM). KA-induced neurotoxic signs as shown by mortality and seizure activity were more accentuated in the SAM-P8 than in the SAM-R1. Levels of MDA and carbonyl are consistently higher in the hippocampus of SAM-P8 than that of SAM-R1. Significant increases in the values of MDA and carbonyl were observed 4 h or 2 days after the final KA administration. This finding was more pronounced in the SAM-P8 than in the SAM-R1. Although a significant loss of hippocampal neurons was observed 7 days post-KA, at this time the MDA and carbonyl content had returned to near control levels. In contrast, fluorescent lipofuscin-like substances and lipofuscin granules were significantly increased 7 days after KA treatments. Therefore, our data suggests that mice in the senescence model are more susceptible to KA-induced seizures/oxidative damage, and that oxidative damage could be one of the casual factors in the accumulation of lipofuscin.

Original languageEnglish
Pages (from-to)211-220
Number of pages10
JournalBehavioural Brain Research
Volume131
Issue number1-2
DOIs
Publication statusPublished - 2002 Apr 11
Externally publishedYes

Keywords

  • Hippocampus
  • Kainic acid
  • Lipofuscin
  • Oxidative stress
  • Seizures
  • Senescence-accelerated mouse

ASJC Scopus subject areas

  • Behavioral Neuroscience

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  • Cite this

    Kim, H. C., Bing, G., Jhoo, W. K., Kim, W-K., Shin, E. J., Park, E. S., Choi, Y. S., Lee, D. W., Shin, C. Y., Ryu, J. R., & Ko, K. H. (2002). Oxidative damage causes formation of lipofuscin-like substances in the hippocampus of the senescence-accelerated mouse after kainate treatment. Behavioural Brain Research, 131(1-2), 211-220. https://doi.org/10.1016/S0166-4328(01)00382-5