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 C A1 neurons after 5-min ischemia by a histochemical method in the presence o r absence of exogenous cytochrome c. In the CA1 neurons, COX activity witho ut exogenous cytochrome c decreased from 1 h after ischemia, but was restor ed by the addition of exogenous cytochrome c in the following 6 h after isc hemia. These results suggest that it is not COX activity but endogenous cyt ochrome c that is changed in the early phase after ischemia, and that COX a ctivity 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 ce ll-death cascade downstream from cytochrome c. Although pro-caspase-3 was s trongly detected, active caspase-3 was not detected before and until 84 h a fter 5-min ischemia. Our data suggested that delayed neuronal death is like ly to progress via cytochrome c-release but not via caspase-3 activation. ( C) 2000 Elsevier Science Ireland Ltd. All rights reserved.