<b>Induction of Autophagy in the Hippocampus after Hypoxic Ischemic Injury to Neonatal </b><b>Rats </b>
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- Koike Masato
- Department of Cell Biology and Neuroscience Juntendo University Graduate School of Medicine,
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- Kawahara Ai
- Department of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine,
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- Shibata Masahiro
- Department of Morphological Sciences, Kagoshima University Graduate School of Medical and Dental Sciences,
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- Uchiyama Yasuo
- Department of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine,
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<p>Summary. Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. Patterns of H/I injury-induced neuron death using rodent models are considered to be similar to the cases in human H/I encephalopathy. The participation of autophagy in neuron death has been a common feature in neonatal rodent models of H/I brain injury and human H/I encephalopathy when examined by immunochemical approaches for MAP1-LC3. This tendency has also been confirmed in neuronal tissue-specific Atg7 conditional knockout mice. However, while the current rat H/I model that is used for analyzing autophagy results in global damage to the ipsilateral hemisphere, it does not entirely reflect the neuropathological changes that appear in the neonatal mouse H/I model, in which the hippocampus is selectively damaged. The present study established a neonatal rat model of H/I injury with a milder ischemic insult, in which autophagy was involved in the hippocampal CA1 region after H/I injury when examined by electron microscopy, and by immunohistochemical and biochemical analyses of LC3. </p>
収録刊行物
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- Archives of Histology and Cytology
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Archives of Histology and Cytology 77 (1), 13-23, 2017
国際組織細胞学会
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詳細情報 詳細情報について
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- CRID
- 1390001206412153344
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- NII論文ID
- 130005397009
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- ISSN
- 13491717
- 09149465
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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
- Crossref
- CiNii Articles
- KAKEN
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- 使用不可