The glutamate excitotoxicity hypothesis of ischemic cell damage holds that cell damage caused by transient cerebral ischemia is triggered by glutamate, released during ischemia from the intracellular compartment into the synaptic cleft: high extracellular glutamate levels activate ionotropic glutamate receptors, thus inducing an overflow of calcium ions into the neurones and a calcium-induced activation of catabolic processes. However, several arguments (and much of the evidence) in favour of this hypothesis do not bear closer examination. On the other hand, evidence is accumulating that, after transient ischemia, calcium fluxes through ionotropic glutamate receptors of the non-NMDA type may play a major role in the manifestation of ischemic cell damage. Calcium fluxes through non-NMDA receptors are determined by mRNA editing of non-NMDA receptor subunits: calcium fluxes are blocked in the presence of an edited subunit. A possible role of mRNA editing in the development of ischemic cell damage is discussed.