Both the rise in extracellular glutamate concentration and anoxic depolarization in the rat striatum during 15 min of global ischemia and reperfusion were monitored using glutamate biosensor and direct current potential electrodes, respectively. Cerebral blood flow (CBF) was simultaneously monitored with a glutamate biosensor or a direct current potential electrode. Before the onset of ischemia, treatment with N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) decreased CBF, while L-arginine increased CBF. However, neither L-NAME nor L-arginine significantly changed CBF during ischemia and reperfusion compared with vehicle-treated animals. The time-course and extracellular glutamate concentration increase during ischemia and reperfusion among L-NAME-, L-arginine- and vehicle-treated animals were very similar. These results were strengthened by the time-course and amplitude of anoxic depolarization. The study suggests that NO is not an important mediator of glutamate release during ischemia and reperfusion.
Animals Arginine