Résumé :
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Acetylcholinesterase (AChE) plays an essential role in neuromuscular transmission. Not surprisingly, neuromuscular transmission during repetitive nerve stimulation is severely depressed in the AChE knockout mice (KO). However, it was not known whether the deficit in AChE leads to changes in the skeletal muscle fibers. The in vitro contractile properties of postural and locomotor soleus muscles of adult KO and normal (wild type, WT) mice were studied and completed by histological and biochemical analyses. Our results show that muscle weight, cross-sectional area (CSA) of muscle fibres and absolute maximal isometric force were reduced in KO mice as compared to WT mice (p < 0.05). Interestingly, the relative amount of slow myosin heavy chain (MHC-1) in muscle homogenates and the percentage of muscle fibres expressing MHC-1 were both decreased by AChE deficiency (p <0.05). Surprisingly, AChE ablation did not resulted in modifications in twitch kinetic, absolute maximal power, fatigue resistance and citrate synthase activity (p > 0.05), despite the reduced number of slow muscle fibres. In conclusion a deficit in AChE leads to alterations in the structure and function of muscles, a susbtantial part of which are not simply related to the reduced body weight of the KO mice. Therefore, our results suggest that this murine model of congenital myasthenic syndrome with end plate AChE deficiency combines alterations in both neurotransmission and intrinsic muscle properties.
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