Analysis of exo- and endocytosis in the mouse nerve ending in experimental diabetes mellitus

Abstract

Diabetes mellitus (DM) is a systemic disease characterized by changes in many organs and tissues, including the motor system. The processes of exo- and endocytosis in the motor nerve ending of the mouse diaphragm muscle during high-frequency activity in experimental alloxan model of DM were studied. Endplate potentials (EPPs) were recorded using intracellular microelectrodes during single and high-frequency (50 Hz, 1 min) stimulation. In mice with the experimental DM, the amplitude-time parameters of EPPs did not differ from those of the control; however, an increase in EPPs depression and a slower recovery were observed during high-frequency stimulation. Using an endocytosis marker FM 1-43, it was shown that in animals with experimental DM fluorescence intensity of the nerve terminals loaded with the dye by high-frequency stimulation increased that was prevented by 1-azakenpaullone (2 μM), an inhibitor of slow dynamin-1-mediated endocytosis. In addition, in the model animals, the destaining of the pre-loaded nerve terminals during high-frequency (50 Hz) stimulation slowed down. The obtained data indicate that in the experimental first type DM recycling of synaptic vesicles via long path becomes more pronounced and the mechanisms of the vesicular transport are impaired, which was confirmed by methods of mathematical modeling.