Corticosterone-aggravated ischemic neuronal damage in vitro is relieved byvanadate

Preischemic hyperglycemia-aggravated neuronal damage has been postulated to occur via enhanced lactic acidosis. We have hypothesized that preischemic glucose loading induces a short-lived elevation in glucocorticoid release w hich, when combined with ischemia, aggravates the postischemic outcome. Thi s study tested this hypothesis in rat hippocampal slices exposed to 4 min i n vitro ischemia of which 58% exhibited recovery of neuronal function. Howe ver, when corticosterone (CT) was present during ischemia, the recovery of neuronal function decreased in a concentration-dependent manner. At 5 muM, CT reduced the recovery rate to 40% while only 10% of slices recovered when exposed to 20 muM CT. Insulin could not block the effect of CT; however, v anadate improved the postischemic recovery of CT-treated (20 muM) slices to 43%. These results indicate that acute, short exposure to CT can significa ntly exacerbate postischemic outcome and that vanadate can antagonize CT ac tion. NeuroReport 12:1261-1263 (C) 2001 Lippincott Williams & Wilkins.