The influence of electrical stimulation on the amplitude of the action potentials recorded from the mouse nervous system In Vitro was investigated. Brief (1 s) high frequency (100 Hz) stimulation of the sciatic nerve induced a longlasting increase in the amplitude of the compound action potential (CAP). Low frequency (1 Hz) stimulation delivered for 15 min attenuated the antidromically evoked potential recorded from hippocampal slices and CAP recorded from the sciatic nerve. The stimulation-induced decrease in the amplitude of CAP occurred in two phases. While during the first phase the decrease was reversible and calcium-dependent, the second, later phase was irreversible. The experiments with two stimulating electrodes activated separately revealed that the changes in the CAP amplitude were not related to unspecific electrode-tissue interactions. The attenuation in the CAP amplitude was accompanied by an increase and decrease of minimal and maximal thresholds, respectively. The stimulation of the sciatic nerve segments with twin pulses revealed that the velocity of CAP propagation and refractoriness were significantly diminished after LFS application. The stimulation- induced changes in CAP were correlated with decreased sodium channels antibody signal, indicating fall in the number of sodium channels. According to postulated hypothesis, the stimulation-induced influx of Na+ during the first phase intensifies internalization of sodium channels. This amplified endocytosis is accompanied by activation of lysosomal pathways and subsequent hydrolysis of sodium channels leading to irreversible decline in the CAP amplitude. Described results indicate, that axons can contribute to neuronal plasticity.
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