Abstract
Exercise-induced fatigue (EF) is a ubiquitous phenomenon in sports competition and training. It can impair athletes’ motor skill execution and cognition. Corticostriatal synaptic plasticity is considered to be the cellular mechanism of movement control and motor learning. However, the effect of EF on corticostriatal synaptic plasticity remains elusive. In the present study, using field excitatory postsynaptic potential recording, we found that the corticostriatal long-term potentiation (LTP) and long-term depression (LTD) were both impaired in EF mice. To further investigate the cellular mechanisms underlying the impaired synaptic plasticity in corticostriatal pathway, whole-cell patch clamp recordings were carried out on striatal medium spiny neurons (MSNs). MSNs in EF mice exhibited increased spontaneous excitatory postsynaptic current (sEPSC) frequency and decreased paired-pulse ratio (PPR), while with normal basic electrophysiological properties and normal sEPSC amplitude. Furthermore, the N-methyl-D-aspartate (NMDA)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) ratio of MSNs was reduced in EF mice. These results suggest that the enhanced presynaptic glutamate (Glu) release and downregulated postsynaptic NMDA receptor function lead to the impaired corticostriatal plasticity in EF mice. Taken together, our findings for the first time show that the bidirectional corticostriatal synaptic plasticity is impaired after EF, and suggest that the aberrant corticostriatal synaptic plasticity may be involved in the production and/or maintenance of EF.
Highlights
Exercise-induced fatigue (EF) is a reduction in maximal voluntary muscle force that results from intense and prolonged exercise (Gandevia, 2001)
For evoked excitatory postsynaptic current recording, picrotoxin (50 μM) was added in the artificial cerebrospinal fluid (ACSF), a tungsten-stimulating electrode was placed in the white matter, and medium spiny neurons (MSNs) in the dorsolateral striatum were chosen to record
These results indicate that EF impairs NMDA receptordependent Long-term potentiation (LTP) in the corticostriatal pathway
Summary
Exercise-induced fatigue (EF) is a reduction in maximal voluntary muscle force that results from intense and prolonged exercise (Gandevia, 2001). It is not entirely due to the peripheral changes at the level of muscle, an inability of the central nervous system (CNS) to drive. The primary input nucleus of basal ganglia, plays a crucial role in action control and motor skill learning (Di Filippo et al, 2009; Zhai et al, 2017). Repetitive activation of cortical inputs can induce long-term changes of synaptic plasticity in the corticostriatal pathway. Corticostriatal synaptic plasticity plays an important role in regulating the excitatory inputs to the basal ganglia, and is believed to be the cellular substrate for voluntary motor control, motor learning and habit formation (Reynolds and Wickens, 2002; Yin and Knowlton, 2006). Movement disorders including Parkinson’s disease (PD; Bagetta et al, 2010; Paillé et al, 2010), Huntington’s disease (HD; Dalbem et al, 2005; Picconi et al, 2006) and dystonia (Martella et al, 2009) have shown to be associated with abnormal corticostriatal synaptic plasticity
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