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Published on: June 13, 2017
TrkB expression at the neuromuscular junction is reduced during aging
Kirkwood E Personius1, Sara D Parker
1Program in Neuroscience, School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA. kep7@buffalo.edu
Muscle & Nerve
|November 28, 2012
Summary
Reduced tyrosine kinase B (TrkB) expression contributes to age-related muscle weakness by altering acetylcholine receptors (AChRs). Maintaining TrkB signaling may improve muscle function in aging.
Area of Science:
- Neuroscience
- Aging Research
- Muscle Physiology
Background:
- Full-length tyrosine kinase B (TrkB.FL) and truncated TrkB (TrkB.t1) receptors are located at the neuromuscular junction alongside acetylcholine receptors (AChRs).
- Previous research indicates that diminished TrkB expression correlates with age-related changes in AChR structure, impaired neurotransmission, and muscle weakness.
Purpose of the Study:
- To determine if TrkB receptor expression decreases in the soleus muscle during the aging process.
Main Methods:
- Investigated TrkB protein and mRNA expression levels in the soleus muscles of senescent (24-month-old) and younger (3-12-month-old) mice.
- Examined the morphology of AChRs in relation to TrkB expression.
Main Results:
- TrkB protein levels were significantly lower in senescent mice compared to younger mice.
- The reduction in TrkB protein coincided with age-related alterations in AChR morphology.
- TrkB.FL mRNA levels increased in aged mice, but this did not correlate with protein levels, suggesting post-transcriptional regulation.
- TrkB.t1 levels remained unchanged with age.
Conclusions:
- Reduced TrkB protein expression in aging may stem from decreased TrkB.FL mRNA translation or accelerated protein degradation.
- Preserving adequate TrkB signaling presents a potential therapeutic strategy to enhance muscle function in older individuals.
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