Abstract: The brain is an expensive tissue in terms of energy consumption. It composes about 2% of body mass and consumes about 20% of all oxygen and calories (Fedorovich and Waseem, 2018). For neurons, glucose is the primary energy substrate, although they are able to use ketone bodies, pyruvate and lactate (Fedorovich and Waseem, 2018). All these compounds can be metabolized directly in the Krebs cycle, bypassing glycolysis. Hence, they are often termed non-glycolytic energy substrates. Out of all potential non-glycolytic substrates, lactate is the most physiological (Magistretti and Allaman, 2018). Ketone bodies could reach concentrations in blood plasma and cerebrospinal fluid which are sufficient to meet metabolic demands of neurons only under specific non-physiological conditions, e.g., ketogenic diet and starvation, or during suckling. In contrast, the normal plasma level of lactate is about 1.5 mM and can reach 20 mM during intensive physical exercise. This is a very high value and this compound undoubtedly contributes to energy production (Mosienko et al., 2015). The lactate concentration in cerebrospinal fluid increases up to 3 mM during brain ischemia (Mosienko et al., 2015). Therefore, the action of lactate on neurons could have certain pathophysiological consequences. In addition, the concept of astrocyte-neuron lactate shuttle has been developed. According to this concept, glycolysis occurs mainly in astrocytes but not in neurons. Lactate is imported from astrocytes to neurons wherein it is further metabolized in mitochondria. Apart from its metabolic function, lactate possesses a signaling function (Morland et al., 2015; Mosienko et al., 2015; Magistretti and Allaman, 2018).