tors from normal into excitotoxicic functioning the decisive role plays the time coarse of activation of specific
MAP kinase, which is sensitive to the extracellulary factors, ERK 1/2 (extracellulary regulated kinase, isoforms
1 and 2). As it is known, specific agonist of these receptors, N-methyl-D-aspartate (NMDA) challenges the short
term activation of this kinase, which leads not to the neuronal cell death but to cell adaptation, while the neu-
rotoxin homocysteine under the same conditions induces the long term activation of ERK 1/2 kinase and cor-
respondingly leads to the massive cells death. Intracellular buffer of free radicals, neuropeptide carnosine (
-alanyl-L-histidine) transforms the excitotoxic response of the receptors to homocysteine into the normal one,
correspondingly saves the cells from necrotic death. We suppose that the same exitotoxic mechanism takes place
during stroke development resulting in neuronal death, and all the substances, which are able to transform MAPK
activation from the continuous regime into transitory one, might be considered as effective neuron protectors from
the oxidative damage and thus be used in stroke therapy.