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Measuring Neuromuscular Junction Functionality
Published on: August 6, 2017
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Ageing and neurotrophic signalling effects on diaphragm neuromuscular function
Sarah M Greising1, Leonid G Ermilov, Gary C Sieck
1Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
The Journal of Physiology
|January 30, 2015
Summary
Age-related muscle loss (sarcopenia) involves brain-derived neurotrophic factor (BDNF) and its receptor TrkB. Reduced BDNF signaling contributes to neuromuscular decline in aging mice.
Area of Science:
- Neuroscience
- Gerontology
- Muscle Physiology
Background:
- Sarcopenia, age-related muscle loss, has poorly understood mechanisms.
- Brain-derived neurotrophic factor (BDNF) and tropomyosin-related kinase receptor B (TrkB) signaling are hypothesized to influence age-related neuromuscular changes.
Purpose of the Study:
- To investigate the role of BDNF/TrkB signaling in age-related neuromuscular decline.
- To examine the effects of BDNF and TrkB inhibition on muscle function and neuromuscular transmission in aging mice.
Main Methods:
- Male TrkB(F616A) mice were treated with control, BDNF, or 1NMPP1 (a TrkB inhibitor).
- Maximal specific force and neuromuscular transmission failure were assessed at 6, 18, and 24 months of age.
- 1NMPP1 inhibits TrkB kinase activity via a specific mutation.
Main Results:
- Maximal force decreased significantly at 24 months compared to younger ages.
- Neuromuscular transmission failure increased with age (18 and 24 months vs. 6 months).
- BDNF treatment improved neuromuscular transmission at 6 and 18 months, while 1NMPP1 impaired it at 6 months.
Conclusions:
- Age-related neuromuscular transmission failure is linked to BDNF/TrkB signaling.
- Inhibition of TrkB kinase activity mimics age-related neuromuscular decline.
- An age-related decrease in endogenous BDNF may precede reduced TrkB kinase activity in the diaphragm.
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