title: Autophagic neuron death in neonatal brain ischemia/hypoxia.
abstract: Hypoxia/ischemia (H/I) brain injury at birth is an important cause of cerebral palsy, mental retardation, and epilepsy. The H/I insult also causes energy failure, oxidative stress, and unbalanced ion fluxes, leading to high induction of autopahgy in brain neurons. Since the mice unable to execute autophagy (due to brain-specific deletion of Atg7 or Atg5) die by massive loss of cerebral and cerebellar neurons with accumulation of ubiquitin aggregates, induction of neuronal autophagy after H/I injury is generally considered neuroprotective by maintaining cellular homeostasis. However, our recent results show that hippocampal pyramidal neurons undergoing caspase-dependent or -independent death following neonatal H/I injury possess abundant LC3-positive granules, and such H/I neuronal death is largely prevented by Atg7 deficiency. In the present review we discuss the roles of autophagy and other forms of programmed cell death in the neonatal H/I brain insult.
authors.affiliation: Department of Cell Biology and Neuroscience, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. y-uchi@anat1.med.osaka-u.ac.jp
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Uchiyama
authors.forename: Masato
authors.initials: M
authors.lastname: Koike
authors.forename: Masahiro
authors.initials: M
authors.lastname: Shibata
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001343:Autophagy; D020169:Caspases / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007231:Infant, Newborn; D009474:Neurons / Q000166:cytology / Q000502:physiology*
chemical_list: D020169:Caspases