Abstract
In young rat cerebellar slices, histological methods showed that the neurotoxic potency of N- methyl- d-aspartate (NMDA) towards granule cells and intracerebellar nucleus neurons was increased 2- to 3-fold on removal of Mg ions, which have a blocking effect on NMDA-activated ion channels. The depolarizing potency of NMDA on granule cells, recorded using a gap method, was similarly enhanced whereas that of kainate, a non-NMDA receptor agonist, was unchanged. The neurotoxic potency of kainate (towards Golgi cells) was also unaltered by removal of Mg 2+. In Mg 2+-containing medium, neuronal depolarization induced either by kainate or by high K + potentiated NMDA toxicity, apparently by reducing the channel block by Mg 2+. The results strongly support the hypothesis that excessive Ca 2+ influx through NMDA/Mg 2+-gated ion channels mediates NMDA toxicity. They also have clear implications regarding the likely mechanism of toxicity of agonists, such as glutamate, able to activate both NMDA and non-NMDA receptors.
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