Abstract
Bilateral occlusion of the carotid arteries of Mongolian gerbils for 10 min. resulted in a consistent pattern of degeneration of hippocampal CA1 neurons. Administration of the non-competitive NMDA antagonist ketamine (100 mg/kg intraperitoneally) 30 min. before the occlusion almost entirely prevented degeneration of CA1 neurones. Indomethacin 5 mg/kg intraperitoneally had no influence on the degeneration, either administered 30 min. before or 15 min. after occlusion. The production of prostaglandins from the NMDA receptor stimulation does not seem to be crucial for the development of the ischaemic lesions at least in the hours immediately following occlusion. Indomethacin did not reduce the anti-ischaemic effect of ketamine in the doses presumably necessary to reduce the increase in intracranial pressure induced by ketamine.
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