Internucleosomal DNA cleavage involved in ischemia-induced neuronal death.
Pyramidal neurons of the hippocampal CA1 are known to be particularly vulnerable to transient ischemia resulting in "delayed neuronal death". Recent studies using aurintricarboxylic acid suggested that ischemia- or excitotoxin-induced neuronal death should share intracellular mechanisms in common with apoptosis. It is, however, unclear about involvement of endonucleases. Here using a transient (5 min) forebrain ischemia model in gerbils, we found that internucleosomal DNA fragmentation developed between 48 and 54 hr recirculations, accompanied with simultaneous or slightly preceding destruction of microtubule-associated protein 2. These results suggest that endonucleases, maybe activated by elevated intracellular Ca2+, play an important role in delayed neuronal death as well as in apoptosis.
Okamoto
M
M
First Department of Internal Medicine, Osaka University School of Medicine, Japan.
Matsumoto
M
M
Ohtsuki
T
T
Taguchi
A
A
Mikoshiba
K
K
Yanagihara
T
T
Kamada
T
T
D000818:Animals; D016923:Cell Death; D004247:DNA / Q000302:isolation & purification / Q000378:metabolism*; D004587:Electrophoresis, Agar Gel; D005260:Female; D005849:Gerbillinae; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D008869:Microtubule-Associated Proteins / Q000032:analysis / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D009707:Nucleosomes / Q000378:metabolism*; D011712:Pyramidal Tracts / Q000187:drug effects / Q000378:metabolism*; D013997:Time Factors
D008869:Microtubule-Associated Proteins; D009707:Nucleosomes; D004247:DNA