<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,
  • Kawahara Ai
    Department of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine,
  • Shibata Masahiro
    Department of Morphological Sciences, Kagoshima University Graduate School of Medical and Dental Sciences,
  • 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>

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