title: [Ischemic axonal injury and its recovery after focal cerebral ischemia].
abstract: After focal cerebral infarction by occluding the middle cerebral artery (MCA) of the rat, the neuronal death occurred in the ipsilateral thalamic neurons, because axons of the thalamic neurons were injured by infarction and retrograde degeneration occurred in the thalamic neurons. However, cortical neurons adjacent to the infarction survived despite their axons injured by ischemia. We employed immunohistochemical staining for 200 kilodalton (kD) neurofilament (NF), in order to study those responses of cortical and thalamic neurons against axonal injury caused by focal cerebral infarction. In the sham operated rats the immunoreactivity to the anti-200 kD NF antibody was only detected in the axon but not in the cell bodies and dendrites. At 3 days after MCA occlusion, axonal swelling proximal to the site of ischemic injury was found in the caudoputamen and internal capsule of the ipsilateral side. At 7 days after occlusion, cell bodies and dendrites of the neurons in the ipsilateral cortex and thalamus were strongly stained with anti-NF antibodies. At 2 weeks after occlusion these responses disappeared in the cortex, but lasted in the thalamus. These phenomena are caused by stasis of the slow axonal transport, because the NF is transported by slow axonal transport. In the cortical neurons impairment of slow axonal transport recovered in the early phase after injury, but in the thalamic neurons the impairment prolonged up to 3 weeks after occlusion. The early recovery of axonal transport from ischemia seemed to be essential for survival of neurons after ischemic axonal injury.
authors.affiliation: Department of Neurosurgery, Toyonaka Municipal Hospital, Osaka, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Taguohi
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Hayakawa
authors.forename: K
authors.initials: K
authors.lastname: Katoka
authors.forename: E
authors.initials: E
authors.lastname: Komura
authors.forename: K
authors.initials: K
authors.lastname: Nakao
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Mogami
authors.forename: N
authors.initials: N
authors.lastname: Kanai
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology* / Q000502:physiology; D001692:Biological Transport; D002470:Cell Survival; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002544:Cerebral Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007124:Immunoenzyme Techniques; D007381:Intermediate Filament Proteins / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009410:Nerve Degeneration; D009416:Nerve Regeneration; D009474:Neurons / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D013788:Thalamus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D007381:Intermediate Filament Proteins