Aim. To study the changes of neurotrophic factors concentrations depending on stage of intoxication with deprivation substances (ethanol or sodium oxybutirate) in rats. Methods. Experiments were performed on male white laboratory rats. Control and experimental groups included 10 animals each. Half-lethal doses of a deprivation substance (ethanol or sodium oxybutirate) were introduced intraperitoneally 3, 6, 12, 24 and 72 hours before blood specimen collection. Neuron-specific enolase, S-100 protein, brain-derived neurotrophic factor, pigment epithelium-derived factor, glial fibrillary acidic protein serum levels were measured by enzyme immunoassay. Results. At single infusion of mean lethal dose of sodium oxybutyrate S-100 protein serum level significantly increased after 6 hours compared to control and stayed elevated during the first 24 hours. The levels of neurotrophic and neuroprotective factors also significantly increased 3 and 6 hours after the drug administration. The toxic dose of ethanol have significantly increased (over than 1.8 times compared to the controls) the concentration of protein S-100 in rats after 3 hours. The maximum increase in the protein S-100 level (by 2.6 times and over) was noted 12 hours after the toxicant administration. Glial fibrillar acidic protein concentration was 2.9 times higher compared to controls 3 hours after and 1.9 times higher 6 hours after higher the ethanol administration (р 0.05). The concentration of brain - derived neurotrophic factor has also increased from 3 to 12 hours after the toxicant administration, and was 2.1 to 2.4 times higher compared to intact animals. Conclusion. Studying of neurotrophic factors brain in plasma showed that the development of hypoxia, accompanying coma, leads to higher serum levels of S-100 protein, brain-derived neurotrophic factor and glial fibrillar acidic protein. The increase in the concentration of S-100 is a marker for the presence of brain damage. The observed increase of glial fibrillar acidic protein in experiments with ethanol may indicate its more severe brain tissue damage compared to sodium oxybutyrate.