CALCIUM INFLUX FROM THE EXTRACELLULAR-SPACE PROMOTES NADH HYPEROXIDATION AND ELECTRICAL DYSFUNCTION AFTER ANOXIA IN HIPPOCAMPAL SLICES

Citation
Ma. Perezpinzon et al., CALCIUM INFLUX FROM THE EXTRACELLULAR-SPACE PROMOTES NADH HYPEROXIDATION AND ELECTRICAL DYSFUNCTION AFTER ANOXIA IN HIPPOCAMPAL SLICES, Journal of cerebral blood flow and metabolism, 18(2), 1998, pp. 215-221
Citations number
53
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism",Hematology
ISSN journal
0271-678X
Volume
18
Issue
2
Year of publication
1998
Pages
215 - 221
Database
ISI
SICI code
0271-678X(1998)18:2<215:CIFTEP>2.0.ZU;2-X
Abstract
A characteristic event during reperfusion after cerebral ischemia in v ivo, and reoxygenation after anoxia in vitro, is hyperoxidation of the electron carriers of the mitochondrial respiratory chain. Current stu dies have tested the hypothesis that there is a relation among calcium molecules derived from extracellular sources, mitochondrial hyperoxid ation, and electrical recovery after anoxia in hippocampal slices. Rat hippocampal slices were superfused with artificial cerebrospinal flui ds (ACSF) containing calcium chloride (CaCl2 in concentrations of: 0.5 , 1, 2, and 4 mmol/L. Slices were made anoxic and then allowed to reco ver for 60 minutes. Reduction-oxidation shifts of NADH were measured b y rapid-scanning spectrofluorometry. Synaptic activity was indicated b y population spike amplitudes in the CA, pyramidal cell subfield of th e hippocampus response to stimulation of the Schaffer collaterals. Low calcium ACSF concentrations ameliorated NADH hyperoxidation and impro ved synaptic transmission recovery after anoxia. High calcium ACSF con centrations had opposite effects. These data suggest a link between mi tochondrial hyperoxidation and electrical recovery after postanoxia re oxygenation and support the hypothesis that cytosolic calcium overload promotes mitochondrial hyperoxidation and limits electrical recovery.