ACTION OF STOBADIN ON GLUTAMATERGIC SYSTE M IN RAT-BRAIN AFTER LOCAL ISCHEMIA

The action of stobadin, a new highly effective antioxidant, on glutama tergic neurotransmission in normal and ischemic rat brain have been st udied. The basal release of L-[C-14]glutamate from brain slices did no t change in the presence of 100 mu M of stobadin, but the K+-stimulate d Ca2+-dependent release of the amino acid was inhibited. An enhanced Ca2+-independent release of exogenous glutamate was observed in ischem ic brain slices, though the K+-stimulated exocytosis of L-[C-14]glutam ate was diminished to 58,4% of control and 74,5% of control in ischemi c brain cortex and hyppocampus, respectively. The rate of exogenous gl utamate uptake into ischemic brain synaptosomes tends to decrease in t he presence of 1-100 mu M stobadin, but no reliable changes could be r egistered as compared with control. The Na+/Ca2+-antiporter was not af fected by stobadin in both normal and ischemic brain synaptosomes. It was concluded that stobadin has no essential action on the studied sys tems after 15-min ischemia. However, its action may be more effective during a reperfusion period when its protective properties are the hig hest.