Journal
AGE
Volume 38, Issue 4, Pages 259-272Publisher
SPRINGER
DOI: 10.1007/s11357-016-9937-7
Keywords
Skeletal muscle; Ageing; Lengthening contractions; Regeneration; Innervation neuromuscular junction
Categories
Funding
- Research into Ageing/Age UK
- Medical Research Council
- Wellcome Trust
- United States National Institute on Aging [AG-20591]
- BBSRC [BB/L021668/1, BB/I004076/1, BB/K003860/1] Funding Source: UKRI
- MRC [MR/M012573/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K003860/1, BB/I004076/1, BB/L021668/1] Funding Source: researchfish
- Medical Research Council [MR/M012573/1] Funding Source: researchfish
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Skeletal muscles of old mice demonstrate a profound inability to regenerate fully following damage. Such a failure could be catastrophic to older individuals where muscle loss is already evident. Degeneration and regeneration of muscle fibres following contraction-induced injury in adult and old mice are well characterised, but little is known about the accompanying changes in motor neurons and neuromuscular junctions (NMJs) following this form of injury although defective re-innervation of muscle following contraction-induced damage has been proposed to play a role in sarcopenia. This study visualised and quantified structural changes to motor neurons and NMJs in Extensor digitorum longus (EDL) muscles of adult and old Thy1-YFP transgenic mice during regeneration following contraction-induced muscle damage. Data demonstrated that the damaging contraction protocol resulted in substantial initial disruption to NMJs in muscles of adult mice, which was reversed entirely within 28 days following damage. In contrast, in quiescent muscles of old mice, similar to 15 % of muscle fibres were denervated and similar to 80 % of NMJs showed disruption. This proportion of denervated and partially denervated fibres remained unchanged following recovery from contraction-induced damage in muscles of old mice although similar to 25 % of muscle fibres were completely lost by 28 days post-contractions. Thus, in old mice, the failure to restore full muscle force generation that occurs following damage does not appear to be due to any further deficit in the percentage of disrupted NMJs, but appears to be due, at least in part, to the complete loss of muscle fibres following damage.
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