Transport mechanism of L-[14C]glutamate in cortical slices and synaptosomes of rabbits exposed to brain ischemia and reperfusion
- 18 Downloads
Changes in the functioning of the glutamatergic system in rabbit brain were studied after partial brain ischemia and reperfusion. In vitro studies were conducted relating to the release of L-[14C]glutamate from cortical brain slices, L-[14C]glutamate uptake in synaptosomes, and45Ca uptake in synaptosomes. It was found that basal release of L-[14C]glutamate from rabbit brain cortical slices after 30 min of partial ischemia and 1 d of reperfusion was essentially without change compared to the control values. After 3 d of reperfusion, there was an increase in basal release of L-[14C]glutamate from rabbit brain cortical slices. K+ stimulated release of L-[14C]glutamate in normal Krebs-Ringer medium was essentially the same in the control group and in the experimental group after 30 min of ischemia. The K+ stimulated release of L-[14C]glutamate independent of calcium was increased to 145% after 30 min of ischemia and 1 d of reperfusion. The decreasedKm value at the glutamate transporter may have contributed to this difference. Kinetic parameters of the L-[14C]glutamate uptakeKm andVmax) in synaptosomes from rabbit brain were significantly lower after 30 min of ischemia. The authors discovered that during the reperfusion period,Vmax 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 control values after 30 min of ischemia and 72 h of reperfusion. According to our results, increased L-[14C]glutamate release after 30 min of ischemia appears to be the result of higher intracellular calcium concentration and possibly also of a higher uptake of glutamate.
Index EntriesBrain ischemia reperfusion glutamate Na+/Ca2+ exchanger synaptosomes brain slices
ethylene glycol-bis(β-aminoethyl ether),N,N,N’,N’-tetraacetic acid
voltage-sensitive calcium channels
Unable to display preview. Download preview PDF.
- Janoff A. S. and Miller K. W. (1982) A critical assessment of the lipid theories of general anaesthetic action, inBiological Membranes, vol. 4 (Chapman D., ed.), Academic, New York, pp. 417–476.Google Scholar
- Kauppinen R. A., McMahon H. T., and Nicholls D. G. (1988) Ca2+-dependent and Ca2+-independent glutamate release, energy status and cytosolic free Ca2+ concentration in isolated nerve terminals following metabolic inhibition: possible relevance to hypoglycaemia and anoxia.Neuroscience 27, 175–182.CrossRefPubMedGoogle Scholar