【摘 要】
：
Fatigue is an everyday life phenomenon.It is induced by motor exercise and characterized by a decrease of muscle force.It occurs in the muscle and in the central nervous system.The "Central" component
【机 构】
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Department of Neuroscience and Pharmacology University of Copenhagen Denmark
【出 处】
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BIT`s 3rd Annual World Congress of NeuroTalk-2012(2012第三届国际神
论文部分内容阅读
Fatigue is an everyday life phenomenon.It is induced by motor exercise and characterized by a decrease of muscle force.It occurs in the muscle and in the central nervous system.The "Central" component of fatigue results in a decrease of the motoneuronal output and hence a decrease of the muscle contraction.Studies in humans have shown that central fatigue is partly due to a decrease of the gain of motoneurons.Several indirect evidences indicate that central fatigue is induced by serotonin (5-HT).However, the cellular mechanisms remain unknown.Our goal is to elucidate these mechanisms.Since the release of 5-HT is correlated to the level of motor exercise, we tested if a massive release of 5-HT induced central fatigue.Because of its high resistance to anoxia, we used the adult turtle as a model of investigation.In an isolated carapace-spinal cord preparation that can generate reproducible scratch reflexes, we found that the amplitude of motor behaviours was reduced after a prolonged synaptic release of 5-HT.This effect disappeared in presence of the 5-HT1A receptor (5-HT1AR) antagonist WAY100635.To investigate the cellular mechanisms involved, we used a slice preparation of the spinal cord.We applied 5-HT or agonists for 5-HTR on different compartments ofmotoneurons (MNs) by means of a microiontophoresis electrode.The release of 5-HT1AR agonist on the axon initial segment (AIS) induced a failure of action potential generation by inhibiting a Na+ current.This effect was specific for the AIS.Immunohistochemical stainings demonstrated 5-HT synaptic boutons on the somatodendritic membrane of MNs but not on the AIS.For this reason we suggest that the 5-HT1AR at the AIS are activated by a spillover mechanism during massive release of 5-HT from synaptic boutons.We propose that, during a prolonged motor exercise, the increase of 5-HT activates 5-HT1AR at the AIS of MNs.Those receptors inhibit the firing of the cell and thereby the contraction of muscles.
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