Abstract
We examined whether age-related differences in N-methyl- d-aspartate (NMDA) receptor-mediated neurotoxicity contribute to the increased vulnerability of the aged brain to anoxic damage. In both adult and aged hippocampal slices, NMDA receptor blockade with MK-801 did not affect the onset of anoxic depolarization. MK-801 improved the postanoxic recovery of synaptic transmission by the same percentage in both age groups. Thus, the faster onset of anoxic depolarization and diminished postanoxic recovery of synaptic transmission seen in aged hippocampal slices cannot be attributed to age-related differences in NMDA receptor-mediated neurotoxicity.
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