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Synaptic terminal glutamate-induced Ca 2+ transients activate neuronal nitric oxide synthase (nNOS)-mediated NO generation, and additionally, Ca 2+ overloaded in the mitochondria induces O 2 /H 2 O 2 generation which can lead to ONOO production and excitotoxicity [18,19,20]

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Data were collected by the unit supervisors during the scheduled check-ups according to the usual clinical practice