Amino acid and purine release in rat brain following temporary middle cerebral artery occlusion
Excitatory amino acid release and neurotoxicity in the ischemic brain may be reduced by endogenously released adenosine which can modulate both glutamate or aspartate release and depress neuronal excitability. The present study reports on the patterns of release of glutamate and aspartate; the inhibitory amino acids GABA and glycine; and of the purine catabolites adenosine and inosine from the rat parietal cerebral cortex during 20 and 60 min periods of middle cerebral artery (MCA) occlusion followed by reperfusion. Aspartate and glutamate efflux into cortical superfusates rose steadily during the period of ischemia and tended to increase even further during the subsequent 40 min of reperfusion. GABA release rose during ischemia and declined during reperfusion, whereas glycine efflux was relatively unchanged during both ischemia and reperfusion. Adenosine levels in cortical superfusates rose rapidly at the onset of ischemia and then declined even though MCA occlusion was continued. Recovery to pre-occulusion levels was rapid following reperfusion. Inosine efflux also increased rapidly, but its decline during reperfusion was slower than that of adenosine.
Key WordsMiddle cerebral artery occlusion cerebral ischemia amino acids adenosine cortical infarction
Unable to display preview. Download preview PDF.
- 1.Choi, D. W. 1991. Calcium and excitotoxic neuronal injury. J. Neurol. Sci. 106:115–122.Google Scholar
- 5.Takagi, K., Ginsberg, M. D., Globus, M. Y.-T., Dietrich, W. D., Martinez, E., Kraydieh, S., and Busto, R. 1993. Changes in amino acid neurotransmitters and cerebral blood flow in the ischemic penumbral region following middle cerebral artery occlusion in the rat: Correlation with histopathology. J. Cereb. Blood Flow Metabol. 13:575–585.Google Scholar
- 8.Hillered, L., Hallstrom, A., Segersvard, S., Persson, L., and Ungerstedt, U. 1989. Dynamics of extracellular metabolites in the striatum after middle cerebral artery occlusion in the rat monitored by intracerebral microdialysis. J. Cerebr. Blood Flow Metabol. 9:607–616.Google Scholar
- 10.Matsumoto, K., Graf, R., Rosner, G., Taguchi, J., and Heiss, W-D. 1993. Elevation of neuroactive substances in the cortex of cats during prolonged focal ischemia. J. Cerebr. Blood Flow Metabol. 13:586–594.Google Scholar
- 13.Phillis, J. W., Walter, G. A., and Simpson, R. E. 1991. Release of purines and neurotransmitter amino acids into cerebral cortical perfusates during and following transient ischemia. Int. J. Purine Pyrimid. Res. 2:41–48.Google Scholar
- 18.Phillis, J. W., and Sen, S. Oxypurinol attenuates hydroxyl radical production during ischemia/reperfusion injury of the rat cerebral cortex: an ESR study. Brain Res. 628:309–312.Google Scholar
- 19.Sen, S., and Phillis, J. W. 1993. Alpha-phenyl-tert-butyl-nitrone (PBN) attenuates hydroxyl radical production during ischemia-reperfusion injury of rat brain: an EPR study. Free Rad. Res. Commun. 19:255–265.Google Scholar
- 23.Rudolphi, K. A., Schubert, P., Parkinson, F. E., and Fredholm, B. B. 1992. Neuroprotective role of adenosine in cerebral ischaemia. Trends in Pharm. Sci. 13:439–445.Google Scholar
- 24.Rudolphi, K. A., Keil, M., and Hinze, H. J. 1987. Effect of theophylline on ischemically induced hippocampal damage in Mongolian gerbils: a behavioral and histopathological study. J. Cerebr. Blood Flow Metabol. 7:74–81.Google Scholar