Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis

H Benveniste, J Drejer, A Schousboe… - Journal of …, 1984 - Wiley Online Library
H Benveniste, J Drejer, A Schousboe, NH Diemer
Journal of neurochemistry, 1984Wiley Online Library
Rats were implanted with 0.3‐mm‐diameter dialysis tubing through the hippocampus and
subsequently perfused with Ringer's solution at a flow rate of 2 (μ1/min. Samples of the
perfusate representing the extracellular fluid were collected over 5‐min periods and
subsequently analyzed for contents of the amino acids glutamate, as‐partate, glutamine,
taurine, alanine, and serine. Samples were collected before, during, and after a 10‐min
period of transient complete cerebral ischemia. The extracellular contents of glutamate and …
Abstract
Rats were implanted with 0.3‐mm‐diameter dialysis tubing through the hippocampus and subsequently perfused with Ringer's solution at a flow rate of 2 (μ1/min. Samples of the perfusate representing the extracellular fluid were collected over 5‐min periods and subsequently analyzed for contents of the amino acids glutamate, as‐partate, glutamine, taurine, alanine, and serine. Samples were collected before, during, and after a 10‐min period of transient complete cerebral ischemia. The extracellular contents of glutamate and aspartate were increased, respectively, eight‐and threefold during the ischemic period; the taurine concentration also was increased 2.6‐fold. During the same period the extracellular content of glutamine was significantly decreased (to 68% of the control value), whereas the concentrations of alanine and serine did not change significantly during the ischemic period. The concentrations of γ‐aminobutyric acid (GABA) were too low to be measured reliably. It is suggested that the large increase in the content of extracellular glutamate and aspartate in the hippocampus induced by the ischemia may be one of the causal factors in the damage to certain neurons observed after ischemia.
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