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Excitatory Amino Acid Neurotransmission and Protection Against Ischaemic Brain Damage

  • Brian Meldrum
  • Mary Evans
  • Jeanette Swan
Part of the Advances in Behavioral Biology book series (ABBI, volume 35)

Summary

Studies of the early cytological changes and the pattern of intracellular accumulation of calcium have suggested that the selective neuronal loss seen in the hippocampus after a transient period of cerebral ischaemia depends in part on excessive excitation occurring during the reperfusion period. In the rat occlusion of the common carotid artery for 10 min combined with arterial hypotension is followed by loss of the majority of CA1 pyramidal cells assessed after 7 days. The focal or systemic injection of 2-amino-7-phosphono-heptanoate, a selective antagonist at the N-methyl-D-aspartate receptor, prior to and at 4 and 10 h after the ischaemia gives partial protection against this cell loss. Non-competitive antagonists acting on the NMDA receptor (such as ketamine and MK 801) also prevent delayed cell loss. The adenosine agonist, 2-chloroadenosine, protects against cell loss when focally injected in the hippocampus.These data provide strong evidence that excitatory transmission at the NMDA receptor during the first 24 h of reperfusion contributes significantly to selective neuronal loss after ischaemia. A novel therapeutic approach to cerebral ischaemia is indicated.

Keywords

NMDA Receptor Status Epilepticus Middle Cerebral Artery Occlusion Excitatory Amino Acid Burst Firing 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • Brian Meldrum
    • 1
  • Mary Evans
    • 1
  • Jeanette Swan
    • 1
  1. 1.Department of NeurologyInstitute of PsychiatryLondonUK

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