The paper represents a literature review devoted to the mechanisms of neurons death in the area of ischemia. The generation of both free radicals and peroxinitrites intensifies when there is a restoration of blood supply through the nidus of ischemic lesion and steadily results in necrosis and apoptosis of cortical neurons. Protective mechanisms include glutamate utilization with neuroglial cells, induction of neuronal-form nitrooxidesynthase, superoxide dismutase, neurotrophins and antiapoptotic enzymes. At separate neurons and synapses level, the aforementioned mechanisms are realized by way of local regulation of hemodynamics, which is mediated by neurovasal messengers and neurotransmitters. The balance of neurotoxic and cytoprotective actions determines selective resistance of separate neuron chemotypes to hypoxia and oxidizing stress that in prospects can serve as a basis for elaborating the directional pharmacological correction of the preceding abnormalities.