Histochemical cytochrome c oxidase activity and caspase-3 in gerbil hippocampal CA1 neurons after transient forebrain ischemia.
We examined the cytochrome c oxidase (COX) activity in gerbil hippocampal CA1 neurons after 5-min ischemia by a histochemical method in the presence or absence of exogenous cytochrome c. In the CA1 neurons, COX activity without exogenous cytochrome c decreased from 1 h after ischemia, but was restored by the addition of exogenous cytochrome c in the following 6 h after ischemia. These results suggest that it is not COX activity but endogenous cytochrome c that is changed in the early phase after ischemia, and that COX activity begins to decrease 9 h after ischemia. We examined caspase-3 in the CA1 region by immunoblotting, as caspase-3 is known to take part in the cell-death cascade downstream from cytochrome c. Although pro-caspase-3 was strongly detected, active caspase-3 was not detected before and until 84 h after 5-min ischemia. Our data suggested that delayed neuronal death is likely to progress via cytochrome c-release but not via caspase-3 activation.
Nakatsuka
H
H
Department of Neurological Surgery, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, Ehime, Japan. hinakats@m.ehime-u.ac.jp
Ohta
S
S
Tanaka
J
J
Toku
K
K
Kumon
Y
Y
Maeda
N
N
Sakanaka
M
M
Sakaki
S
S
D000818:Animals; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism*; D016923:Cell Death; D003576:Electron Transport Complex IV / Q000378:metabolism*; D005849:Gerbillinae; D006624:Hippocampus / Q000201:enzymology* / Q000473:pathology; D006651:Histocytochemistry; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000473:pathology; D008297:Male; D009474:Neurons / Q000201:enzymology* / Q000473:pathology; D016548:Prosencephalon / Q000201:enzymology* / Q000473:pathology
D003576:Electron Transport Complex IV; D053148:Caspase 3; D020169:Caspases