Abstract：
:Denervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by denervation. Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and connexin45 hemichannels, which promote muscle atrophy. In co-culture studies, connexin43/45 hemichannel knockout or knockdown increased innervation of muscle fibers by dorsal root ganglion neurons. Our results show that ACh released by motoneurons exerts a hitherto unknown function independent of myofiber contraction. nAChRs and connexin hemichannels are potential molecular targets for therapeutic intervention in a variety of pathological conditions with reduced synaptic neuromuscular transmission.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Cisterna BA,Vargas AA,Puebla C,Fernández P,Escamilla R,Lagos CF,Matus MF,Vilos C,Cea LA,Barnafi E,Gaete H,Escobar DF,Cardozo CP,Sáez JCdoi
10.1038/s41467-019-14063-8subject
Has Abstractpub_date
2020-02-26 00:00:00pages
1073issue
1issn
2041-1723pii
10.1038/s41467-019-14063-8journal_volume
11pub_type
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