TRANSPORT MECHANISM OF L-[C-14]GLUTAMATE IN CORTICAL SLICES AND SYNAPTOSOMES OF RABBITS EXPOSED TO BRAIN ISCHEMIA AND REPERFUSION

Changes in the functioning of the glutamatergic system in rabbit brain were studied after partial brain ischemia and reperfusion. In vitro s tudies were conducted relating to the release of L-[C-14]glutamate fro m cortical brain slices, L-[C-14]glutamate uptake in synaptosomes, and Ca-45 uptake in synaptosomes. It was found that basal release of L-[C -14]glutamate from rabbit brain cortical slices after 30 min of partia l ischemia and 1 d of reperfusion was essentially without change compa red to the control values. After 3 d of reperfusion, there was an incr ease in basal release of L-[C-14]glutamate from rabbit brain cortical slices. K+ stimulated release of L-[C-14]glutamate in normal Krebs-Rin ger medium was essentially the same in the control group and in the ex perimental group after 30 min of ischemia. The K+ stimulated release o f L-[C-14]glutamate independent of calcium was increased to 145% after 30 min of ischemia and 1 d of reperfusion. The decreased K-m value at the glutamate transporter may have contributed to this difference. Ki netic parameters of the L-[C-14]glutamate uptake (K-m and V-max) in sy naptosomes from rabbit brain were significantly lower after 30 min of ischemia. The authors discovered that during the reperfusion period, V -max was almost the same as in the control group. The activity of the Na+/Ca2+ exchanger in synaptosomes of rat brain was about 70% of the c ontrol values after 30 min of ischemia and 72 h of reperfusion. Accord ing to our results, increased L-[C-14]glutamate release after 30 min o f ischemia appears to be the result of higher intracellular calcium co ncentration and possibly also of a higher uptake of glutamate.