The Role of MCT1 Transporters in the Implementation of the Neuroprotective Effect of Glial Cell-Derived Neurotrophic Factor

The search for new molecular targets to protect brain cells from ischemic damage has remained one of the most urgent tasks of neurobiology and medicine over the past decades. The modern concept of the glucose-lactate shuttle, the main mechanism for providing energy support to neurons under conditions of increased physiological activity, implies a functional fusion of neuron and astrocyte metabolism, which becomes particularly important under energy or oxygen starvation conditions. The transfer of energy substrates in response to increased glutamate release by the presynaptic terminal occurs through monocarboxylate transporters (MCTs) and depends on a large number of endogenous mechanisms of homeostasis. Our work examined the role of MCTs in the implementation of the neuroprotective effect of glial cell-derived neurotrophic factor (GDNF), one of the key participants in the regulatory system capable of maintaining the viability and functional activity of neurons under conditions of energy starvation. It has been shown that the application of the MCT1 transporter inhibitor, even under normal conditions, significantly affects the parameters of spontaneous bioelectrical activity of neural networks and cell viability of primary dissociated hippocampal cultures. However, the authors’ data on the role of this type of transporters in glucose deprivation and the effect of MCT blockade on the neuroprotective effects of GDNF are of the greatest interest.