Esrefoglu, MGepdiremen, AKurus, M2024-08-042024-08-0420030767-39811472-8206https://doi.org/10.1046/j.1472-8206.2003.00149.xhttps://hdl.handle.net/11616/93530Glutamate excitotoxicity has been postulated to underlie the neuronal death that occurs after ischemia. The most sensitive tissues to ischemic injury are hippocampus and cerebellum, whereas cerebrum is more resistant. We studied the glutamate-induced ultrastructural alterations in rat parietal and cerebellar neurons comparatively. We observed that glutamate (45 min, 10(-7) M) causes considerable nuclear, mitochondrial and cytoplasmic changes in both the neuron types. Mitochondrial and nuclear changes were particularly more severe in cerebellar granular, than the ones in parietal neurons. It has been concluded that glutamate induces necrotic changes in both parietal and cerebellar neurons. But cerebellar cortex was found to be more sensitive to glutamate excitotoxicity than cerebral cortex. We suggest that mitochondrial damage is, probably, an important factor in neuron necrosis, which is mediated by glutamate excitotoxicity.eninfo:eu-repo/semantics/closedAccesscerebellumelectron microscopyexcitotoxicitynecrosisneocortexglutamateArticle1733413471280357310.1046/j.1472-8206.2003.00149.x2-s2.0-0037757865Q2WOS:000183797800007Q3