Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats
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- Zhang Lifeng
- Heping District Center for Disease Control and Prevention,China Department of Toxicology, School of Public Health, China Medical University, China Department of Occupational and Environmental Health, School of Public Health, China Medical University, China
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- Jin Cuihong
- Department of Toxicology, School of Public Health, China Medical University, China
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- Liu Qiufang
- Department of Toxicology, School of Public Health, China Medical University, China
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- Lu Xiaobo
- Department of Toxicology, School of Public Health, China Medical University, China
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- Wu Shengwen
- Department of Toxicology, School of Public Health, China Medical University, China
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- Yang Jinghua
- Department of Toxicology, School of Public Health, China Medical University, China
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- Du Yanqiu
- 9th People’s Hospital of Shenyang, China
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- Zheng Linlin
- Medical college, Eastern Liaoning University, China
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- Cai Yuan
- Department of Occupational and Environmental Health, School of Public Health, China Medical University, China Department of Toxicology, School of Public Health, China Medical University, China
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抄録
Epidemiological investigations have indicated that aluminum (Al), as an important environmental neurotoxicant, could cause damage to the cognitive function which was closely related with neurodegenerative diseases. Long-term potentiation (LTP) is one form of synaptic plasticity in association with cognitive function. Previous studies have demonstrated that Al impaired early phase long-term potentiation (E-LTP) in vivo and in vitro. However, Al-induced damage to late phase long-term potentiation (L-LTP) has poorly been studied. The present study was designed to observe the effects of subchronic Al exposure on the spatial memory, hippocampus ultrastructure and L-LTP in rats. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation from parturition to weaning for 3 weeks and then fed with the distilled water containing 0, 0.2%, 0.4% and 0.6% aluminum chloride (AlCl3) respectively from weaning to postnatal 3 months. The levels of Al in blood and hippocampus were quantitated by atomic absorption spectrophotometer. Morris water maze test was performed to study spatial memory. The induction and maintenance of L-LTP in area of Schaffer collateral- CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. Hippocampus was collected for transmission electron microscopy observation. The results showed that the Al concentrations in blood and hippocampus of Al-exposed rats were higher than those of the control rats. Al could impair spatial memory ability of rats. Neuronal and synaptic ultrastructure from Al-exposed rats presented pathological changes; the incidence of L-LTP has a decrease trend while population spike (PS) amplitude was much smaller significantly stimulated by high-frequency stimulation (HFS) in Al-exposed rats. Our findings showed that Al exposure caused spatial memory damage, under which the neuronal and synaptic ultrastructure changes maybe were their morphological basis and the impaired L-LTP of hippocampus could be their electrophysiological basis.
収録刊行物
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- The Journal of Toxicological Sciences
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The Journal of Toxicological Sciences 38 (2), 255-268, 2013
一般社団法人 日本毒性学会
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詳細情報 詳細情報について
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- CRID
- 1390282679881912960
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- NII論文ID
- 10031151429
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- NII書誌ID
- AN00002808
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- COI
- 1:CAS:528:DC%2BC3sXnt12qtb4%3D
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- ISSN
- 18803989
- 03881350
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- NDL書誌ID
- 024645026
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- PubMed
- 23535404
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可