Abstract
The responses of the primary sensory neuron to the effect of subnanomolar and nanomolar concentrations of ouabain, which correspond to its endogenous concentrations (EO), were investigated. By the method of atomic force microscopy (AFM) it was found that the effect of EO led to an increase in the stiffness of the neuron. It was found using the patch-clamp method that due to the ligand-receptor binding of EO to the Na, K-ATPase/Src complex, the effective charge of the activation gating system of NaV1.8 channels decreases. It was also found that EO-activated triggering of the intracellular cascade, in which the Na, K-ATPase/Src complex acts as a signal transducer, leads to a decrease in the fluorescence intensity of antibodies to NaV1.8 channels, which was revealed using confocal laser scanning microscopy. The results obtained allowed us to suggest that EO, triggering the transducer function of the Na, K-ATPase/Src complex and the corresponding intracellular signaling cascade, is able to modulate the expression of the SCN10A gene, which produces the NaV1.8 channels responsible for encoding nociceptive signals.
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