Abstract
Corticostriatal synaptic plasticity is considered to be a cellular basis for somatic motor regulation and motor skill learning. Changes in synaptic transmission efficiency underlie functional plasticity, while structural plasticity involves changes in the ultrastructure of the synapse and the levels of synaptic proteins. Exercise-induced fatigue may impair corticostriatal synaptic plasticity, and this impairment may be an important mechanism for exercise-induced fatigue. However, prior research focused mainly on functional plasticity such that the structural plasticity was not well understood. Because corticostriatal synapses are typical asymmetric synapses, here we have used transmission electron microscopy to examine the changes of asymmetry synaptic ultrastructure in rat striatum before and after repetitive exercise-induced fatigue; we have also used western blotting to detect the levels of synaptic active region protein Munc 13, RIM1 and synaptic vesicle protein Rab3A and postsynaptic density PSD-95 protein in rat striatum before and after exercise-induced fatigue. The results showed that the ultrastructure of asymmetry corticostriatal synapses and synaptic protein levels in the striatum of rats were abnormally changed after repetitive exercise-induced fatigue. These abnormal changes in synaptic ultrastructure and related protein levels may be the structural basis for the corticostriatal plasticity impairment after exercise-induced fatigue.