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Exercise-Induced Fatigue Impairs Bidirectional Corticostriatal Synaptic Plasticity.

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|February 10, 2018
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Exercise-induced fatigue impairs corticostriatal synaptic plasticity, affecting motor control and learning. This study reveals reduced long-term potentiation and depression in fatigued mice, impacting movement and cognition.

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corticostriatal pathwayexercise-induced fatigueglutamate releaselong-term depressionlong-term potentiation

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Area of Science:

  • Neuroscience
  • Exercise Physiology

Background:

  • Exercise-induced fatigue (EF) is common in athletes, impairing motor skills and cognition.
  • Corticostriatal synaptic plasticity underlies movement control and learning, but its response to EF is unknown.

Purpose of the Study:

  • To investigate the impact of EF on corticostriatal synaptic plasticity.
  • To elucidate the cellular mechanisms behind EF-induced changes in synaptic plasticity.

Main Methods:

  • Field excitatory postsynaptic potential recordings in mice to assess long-term potentiation (LTP) and long-term depression (LTD).
  • Whole-cell patch clamp recordings on striatal medium spiny neurons (MSNs) to analyze electrophysiological properties.

Main Results:

  • Both LTP and LTD at corticostriatal synapses were impaired in EF mice.
  • MSNs in EF mice showed increased spontaneous excitatory postsynaptic current (sEPSC) frequency and decreased paired-pulse ratio (PPR).
  • Reduced N-methyl-D-aspartate (NMDA)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) ratio in MSNs indicated downregulated postsynaptic NMDA receptor function.

Conclusions:

  • EF impairs bidirectional corticostriatal synaptic plasticity through enhanced presynaptic glutamate release and reduced postsynaptic NMDA receptor function.
  • Aberrant corticostriatal plasticity may contribute to the development and persistence of exercise-induced fatigue.