Mouse diaphragm at late aging: presynaptic compensation at the neuromuscular junction
In 24- versus 3-month-old mice, aged diaphragm neuromuscular junctions showed weaker postsynaptic responses to single acetylcholine quanta, while presynaptic release, vesicle mobilization and recycling increased, probably partly compensating. [1]
Automatic summary · not editorially reviewed
The key findings
The study compared neuromuscular transmission in the diaphragm of 24-month-old and 3-month-old mice; aged junctions showed a smaller evoked postsynaptic response and a much greater fall in miniature end-plate amplitude. [1]
At aged junctions, spontaneous exocytosis, presynaptic action potential propagation velocity, quantal content after single stimuli and the asynchronous component of evoked release increased, as did exocytosis during 10–70 Hz trains and prolonged intermittent 20-Hz stimulation. [1]
The estimated readily releasable pool and facilitation between bursts increased with age and correlated with less vesicle clustering and weaker synapsin 1 labeling; the authors propose this may partly compensate for the weaker postsynaptic response. [1]
The source at a glance
- Study type / format
- Preclinical mouse study (abstract)
- Population / context
- Diaphragm neuromuscular junctions of 24-month-old and 3-month-old mice
- Summary based on
- Study abstract
- Original publication
- October 3, 2026
Aged versus young mouse diaphragm junctions compared
The diaphragm is the main breathing muscle. The study compared key measures of signal transmission at the neuromuscular junction in the diaphragm of 24-month-old and 3-month-old mice. At aged junctions, the size of the evoked postsynaptic response fell, and the miniature end-plate amplitude fell much more. These are measurements of the muscle-side response, not of how long the animals lived.
Supporting source [1]
More presynaptic release in aged junctions
At aged junctions, spontaneous exocytosis intensity, the speed of presynaptic action potential propagation, the quantal content of end-plate potentials after single stimuli and the asynchronous part of evoked release all increased. Exocytosis of acetylcholine quanta also rose during short stimulus trains at 10–70 Hz and especially during prolonged intermittent 20-Hz nerve stimulation. Facilitation between bursts, a sign of vesicle mobilization, and the estimated readily releasable pool both increased with age.
Supporting source [1]
Vesicle recycling and synapsin 1 in aged junctions
The increase in the readily releasable pool correlated with less vesicle clustering and weaker immunolabeling of synapsin 1, a protein that restrains vesicles in the nonactive pool. Tracking release of the FM1-43 dye from synaptic vesicles suggested a faster vesicle recycling rate during 20-Hz activity in aged junctions. The authors propose that enhanced neurotransmitter release, probably through a larger readily releasable pool and more vesicle mobilization, may partly compensate for the weaker postsynaptic response to a single acetylcholine quantum. They suggest such adaptations are likely needed to preserve diaphragm function with aging.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a mouse study comparing 24- and 3-month-old animals, so the findings describe aged mouse diaphragm junctions, not human lifespan or clinical outcomes. The compensation explanation is proposed by the authors, and the correlations do not establish cause.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Tsentsevitsky AN, Khaziev AN, Sibgatullina GV, Salnikov VV, Tokmakova AR, Khuzakhmetova VF, Odnoshivkina JG, Bukharaeva EA, Petrov AM. · europepmc.org · October 3, 2026