Characterization of transient focal ischemia-induced increases in extracellular glutamate and aspartate in spontaneously hypertensive rats

Characterization of transient focal ischemia-induced increases in extracellular glutamate and... Using middle cerebral artery occlusion (MCAO) and in vivo microdialysis, we have evaluated the changes in extracellular concentrations of the excitatory amino acids (EAA) glutamate and aspartate during varying periods of MCAO (0, 30, 60 min) in the striatum of spontaneously hypertensive rats (SHR). A positive correlation between occlusion time-dependent elevations in EAAs and the resulting ischemic injury was observed. This is the first demonstration of the temporal profile of EAA efflux during transient focal ischemia in SHRs. Possible sources and mechanisms of ischemia-induced EAA efflux were examined during 60 min of MCAO. Removal of Ca 2+ from the microdialysis infusion media significantly attenuated ischemia-induced increases in both glutamate (from ischemic peak of 4892 ± 1298 to 1144 ± 666% of preischemic values) and aspartate (from 2703 ± 682 to 2090 ± 599% of preischemic values). Similarly, infusion of the voltage dependent Na + channel blocker tetrodotoxin (TTX; 10 μM) significantly attenuated MCAO-induced increases in glutamate (to 1313 ± 648%) and aspartate (to 359 ± 114%). Infusion of the GLT-1 selective nontransportable inhibitor, dihydrokainate (DHK; 1mM) also significantly attenuated the ischemia-induced increases in both EAAs (1285 ± 508 and 1366 ± 741% of the preischemic levels, respectively). These results indicate that during transient focal ischemia the increase in extracellular EAAs originates from both the neuronal pool, via conventional exocytotic release, and glial sources via the reversal of the GLT-1 transporter. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Bulletin Elsevier

Characterization of transient focal ischemia-induced increases in extracellular glutamate and aspartate in spontaneously hypertensive rats

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Publisher
Elsevier
Copyright
Copyright © 2001 Elsevier Science Inc.
ISSN
0361-9230
eISSN
1873-2747
D.O.I.
10.1016/S0361-9230(00)00363-4
Publisher site
See Article on Publisher Site

Abstract

Using middle cerebral artery occlusion (MCAO) and in vivo microdialysis, we have evaluated the changes in extracellular concentrations of the excitatory amino acids (EAA) glutamate and aspartate during varying periods of MCAO (0, 30, 60 min) in the striatum of spontaneously hypertensive rats (SHR). A positive correlation between occlusion time-dependent elevations in EAAs and the resulting ischemic injury was observed. This is the first demonstration of the temporal profile of EAA efflux during transient focal ischemia in SHRs. Possible sources and mechanisms of ischemia-induced EAA efflux were examined during 60 min of MCAO. Removal of Ca 2+ from the microdialysis infusion media significantly attenuated ischemia-induced increases in both glutamate (from ischemic peak of 4892 ± 1298 to 1144 ± 666% of preischemic values) and aspartate (from 2703 ± 682 to 2090 ± 599% of preischemic values). Similarly, infusion of the voltage dependent Na + channel blocker tetrodotoxin (TTX; 10 μM) significantly attenuated MCAO-induced increases in glutamate (to 1313 ± 648%) and aspartate (to 359 ± 114%). Infusion of the GLT-1 selective nontransportable inhibitor, dihydrokainate (DHK; 1mM) also significantly attenuated the ischemia-induced increases in both EAAs (1285 ± 508 and 1366 ± 741% of the preischemic levels, respectively). These results indicate that during transient focal ischemia the increase in extracellular EAAs originates from both the neuronal pool, via conventional exocytotic release, and glial sources via the reversal of the GLT-1 transporter.

Journal

Brain Research BulletinElsevier

Published: Dec 1, 2000

References

  • Electrogenic uptake of glutamate and aspartate into glial cells isolated from the salamander (Ambystoma) retina
    Barbour, B.; Brew, H.; Attwell, D.
  • Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis
    Benveniste, H.; Drejer, J.; Schousboe, A.; Diemer, N.H.
  • Calcium accumulation by glutamate receptor activation is involved in hippocampal cell damage after ischemia
    Benveniste, H.; Jorgensen, J.; Diemer, N.H.; Hansen, A.J.
  • Cellular origin of ischemia-induced glutamate release from brain tissue in vivo and in vitro
    Drejer, J.; Benveniste, H.; Diemer, N.H.; Schousboe, A.
  • Protein kinase C modulates ischemia-induced amino acid release in the striatum of hypertensive rats
    Nakane, H.; Yao, H.; Ibayashi, S.; Kitazano, T.; Ooboshi, H.; Uchimura, H.; Fujishima, M.
  • Mechanism of glutamate and aspartate release in the ischemic rat cerebral cortex
    Phillis, J.W.; O’Regan, M.H.
  • Kainic acid inhibits the synaptosomal plasma membrane glutamate carrier and allows glutamate leakage from the cytoplasm but does not affect glutamate exocytosis
    Pocock, J.M.; Murphie, H.M.; Nicholls, D.G.
  • Glutamate and the pathophysiology of hypoxic/ischemic brain damage
    Rothman, S.M.; Olney, J.W.
  • Excitotoxicity and the NMDA receptor
    Rothman, S.M.; Olney, J.W.
  • Real-time monitoring of glutamate transmitter release with anoxic depolarization during anoxic insult in rat striatum
    Satoh, M.; Asai, S.; Katayama, Y.; Kohno, T.; Ishikawa, K.
  • Altered glutamatergic transmission in neurological disorders
    Wahl, F.; Obrenovitch, T.P.; Hardy, A.; Plotkine, M.; Boulu, R.; Symon, N.
  • Brain metabolism of branched-chain amino acids
    Yudkoff, M.

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