作者: Dennis W. Choi
DOI: 10.1016/S0079-6123(08)63263-X
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摘要: Publisher Summary This chapter discusses two distinct hypotheses to explain a greater value of N -methyl- D -aspartate (NMDA) antagonists as neuroprotective agents in focal ischemia compared with global ischemia—including, (1) the toxic potential NMDA receptor overactivation is small, and only critical factor neuronal death under certain special conditions, such partial energy depletion associated ischemic penumbra, (2) The large, but limited by endogenous mechanisms especially active ischemia. Only when receptor-mediated toxicity suppressed does more slowly triggered alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)/kainate receptors become apparent. difference between these rank order versus AMPA/kainate receptors, respect excitotoxic potential. In both hypotheses, occurrence calcium overload suggested trigger neurodegeneration. Because families mediate most fast excitatory synaptic transmission throughout CNS, they may contribute heavily sodium during after an insult, leading subsequently overload.