Abstract

Motor fatigue occurring during prolonged physical activity has both peripheral and central origins. It was previously demonstrated that the excitability of motoneurons was decreased when a spillover of serotonin could activate extrasynaptic 5-HT1A receptors at the axon initial segment (AIS) of motoneurons. Here we investigated the impact of massive synaptic release of serotonin on motor behavior in an integrated preparation of the adult turtle performing fictive scratching behaviors. We found that a prolonged electrical stimulation of the raphe spinal pathway induced a reversible inhibition of the motor behavior that lasted several tens of seconds. The effect disappeared when the spinal cord was perfused with an antagonist for 5-HT1A receptors. By demonstrating a direct impact of serotonin on motor behavior, we suggest a central role of this monoamine behind central fatigue.

Highlights

  • Prolonged physical activity results in the induction of motor fatigue

  • We induced fictive scratching in an integrated preparation consisting of the lumbar spinal cord left intact in the backbone and the carapace of the adult turtle (Alaburda and Hounsgaard, 2003; see ‘‘Materials and Methods’’ section)

  • As for all the preparations tested (n = 4), we found that 1 min after ending dorsolateral funiculus (DLF) stimulation, the amplitude of evoked scratch reflexes was strongly inhibited (Figures 3A–C; mean inhibition to 50 ± 40% of control value; n = 12 trials from four different preparation; p = 0.004; Kruskal-Wallis followed by Dunn’s multiple comparison test)

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Summary

Introduction

Prolonged physical activity results in the induction of motor fatigue. This temporary inability of muscles to operate maximally is caused by physically distinct mechanisms. In subjects maintaining a constant firing rate for a single motor unit for which they receive an audio feedback during a moderate isometric contraction, the force produced by the muscle increases. This shows that during prolonged activity, motoneurons require stronger excitatory inputs to maintain their firing rate (Johnson et al, 2004). It demonstrates that central fatigue does not require strong contractions in order to occur

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