Abstract
In summary then, these findings suggest that specialized pumps remove some Ach from the synapse, as they do for most neurotransmitters. Second, and perhaps most importantly, they at least raise the possibility that the pathophysiology of DMD in humans could be partially attributed to altered cholinergic transmission or kinetics of acetylcholine at the NMJ. These new results are appealing because they suggest a unifying hypothesis that fits well both with recent C. elegans data and with older observations made on vertebrate muscle. © 2005 Nature Publishing Group All rights reserved.
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CITATION STYLE
Ségalat, L., & Anderson, J. E. (2005, January). Duchenne muscular dystrophy: Stalled at the junction? European Journal of Human Genetics. https://doi.org/10.1038/sj.ejhg.5201304
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