Cortical spreading depression affects reactive oxygen species production

Cortical spreading depression (CSD) is a reversible electrophysiological phenomenon that is not associated with tissue damage under normal blood supply. The induction of CSD during ischemia causes an increase in tissue damage, while pre-conditioning with CSD decreases the damage induced by a subsequent episode of ischemia. The mechanisms underlying these effects are not clear. Because the production of reactive oxygen species (ROS) is involved in tissue damage during ischemia–reperfusion, the aim of the present study was to evaluate the effects of CSD on superoxide production (O2−), on hydrogen peroxide (H2O2) production and on superoxide dismutase (SOD) activity in the cerebral cortex. CSD was induced by KCl application on the cortical surface in rats. O2− production was evaluated using dihydroethidium (DHE) that is oxidized to the fluorescent dye ethidium (HEt) by O2−. The extracellular level of H2O2 was evaluated by microdialysis sampling and HPLC analysis. SOD activity was evaluated with a histochemical assay. The results showed an increase in H2O2 production, an increase in SOD activity and a decrease in O2− concentration 1 h after CSD induction.

Research Highlights
► CSD increases superoxide dismutase activity (SOD).
► CSD decreases superoxide ion (O2−).
► CSD increases hydrogen peroxide (H2O2).
► The increased SOD activity could mediate the neuroprotective effect of CSD pre-conditioning by dismutation of O2ˉ to H2O2.