• A Mitani, H Imon, K Iga, H Kubo, and K Kataoka.
• Department of Physiology, The University of Ehime, School of Medicine, Japan.
• Brain Res. Bull. 1990 Aug 1; 25 (2): 319-24.

AbstractIn order to elucidate the role of glutamate in the pathogenesis of delayed neuronal death, we analyzed changes in extracellular levels of glutamate induced by transient ischemia in the Mongolian gerbil hippocampus by a new brain microdialysis method combined with an enzymatic cycling technique. We also studied the effect of this change in glutamate on CA1 spontaneous neuronal discharges. The level of glutamate significantly increased during the 5 min of ischemia and during the first 5 min of recirculation. However, neuronal hyperactivity anticipated as a result of the increased extracellular glutamate was not observed. Spike discharges disappeared during and shortly after 5 min of ischemia; CA1 spontaneous spike discharges reappeared about 15 min after the recirculation. The frequency and amplitude of the discharges of CA1 neurons returned to normal by 30 min of the recirculation. However, the pattern of discharges was different from that recorded before the ischemia. CA1 neurons were found dead 4 days after the ischemia. Brief exposure to toxic concentrations of glutamate may cause the delayed neuronal death.

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