Corticosterone-aggravated ischemic neuronal damage in vitro is relieved by vanadate

• Published in: Neuroreport Vol. 12; no. 6; p. 1261
• Main Authors: Payne, R S, Schurr, A
• Format: Journal Article
• Language: English
• Published: England 08.05.2001
• Subjects: Animals; Anti-Inflammatory Agents - adverse effects; Brain Ischemia - chemically induced; Brain Ischemia - metabolism; Brain Ischemia - pathology; Cell Hypoxia - drug effects; Corticosterone - adverse effects; Dose-Response Relationship, Drug; Glucose - deficiency; Hippocampus - drug effects; In Vitro Techniques; Male; Rats; Rats, Sprague-Dawley; Vanadates - therapeutic use
• DOI: 10.1097/00001756-200105080-00041
• ISSN: 0959-4965

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 which, when combined with ischemia, aggravates the postischemic outcome. This study tested this hypothesis in rat hippocampal slices exposed to 4 min in vitro ischemia of which 58% exhibited recovery of neuronal function. However, when corticosterone (CT) was present during ischemia, the recovery of neuronal function decreased in a concentration-dependent manner. At 5 microM, CT reduced the recovery rate to 40% while only 10% of slices recovered when exposed to 20 microM CT. Insulin could not block the effect of CT; however, vanadate improved the postischemic recovery of CT-treated (20 microM) slices to 43%. These results indicate that acute, short exposure to CT can significantly exacerbate postischemic outcome and that vanadate can antagonize CT action.