Using immunocytochemistry and fluorescence microscopy, it was shown that the expression of the calcium-binding proteins parvalbumin, calbindin and calretinin in GABAergic neurons limited the increase in the level of cytosolic calcium ([Ca2+]i) during the excitotoxic effect of glutamate (GluTox). Under conditions of repeated episodes of hypoxia, Ca2+ oscillations were generated in GABAergic neurons, and the expression of calcium-binding proteins determined the amplitude of hypoxia-induced Ca2+ impulses. Expression of parvalbumin during hypoxia was most effective in suppressing the amplitude of Ca2+ signals. With GluTox, irreversible depolarization of the mitochondria of GABAergic neurons occurred, which lacked calcium-binding proteins, while the expression of parvalbumin, calbindin or calretinin contributed to the preservation of mitochondrial polarization and maintenance of their functioning under the influence of glutamate. At the same time, parvalbumin also turned out to be the most effective calcium-binding protein. As a result, restrictions on the level of [Ca2+]i during GluTox by calcium-binding proteins in GABAergic neurons led to suppression of the production of reactive oxygen species by mitochondria on the one hand, and on the other hand, calcium-binding proteins were able to protect GABAergic neurons from hyperproduction of nitric oxide. Thus, calcium-binding proteins were not only a marker of subtypes of GABAergic neurons, but also determined their physiological parameters under stressor conditions, which can be used to identify the subtype of GABAergic neurons by fluorescent signals of ROS production, nitric oxide, or the kinetics of Ca2+ signals.