Age-related fragmentation of the motor endplate is not associated with impaired neuromuscular transmission in the mouse diaphragm.
As mammals age, their neuromuscular junctions (NMJs) gradually change their form, acquiring an increasingly fragmented appearance consisting of numerous isolated regions of synaptic differentiation. It has been suggested that this remodelling is associated with impairment of neuromuscular transmission, and that this contributes to age-related muscle weakness in mammals, including humans. The underlying hypothesis, that increasing NMJ fragmentation is associated with impaired transmission, has never been directly tested. Here, by comparing the structure and function of individual NMJs, we show that neuromuscular transmission at the most highly fragmented NMJs in the diaphragms of old (26-28 months) mice is, if anything, stronger than in middle-aged (12-14 months) mice. We suggest that NMJ fragmentation per se is not a reliable indicator of impaired neuromuscular transmission.
Novartis Institutes for Biomedical Research, Basel, Switzerland.
Silvia
S
Willadt
Novartis Institutes for Biomedical Research, Basel, Switzerland.
Mark
M
Nash
Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom.
Clarke R
CR
Slater
D000367:Age Factors; D000818:Animals; D003964:Diaphragm / Q000294:innervation* / Q000502:physiology*; D019054:Evoked Potentials, Motor; D008297:Male; D051379:Mice; D009045:Motor Endplate / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D011978:Receptors, Nicotinic / Q000378:metabolism; D009435:Synaptic Transmission
D011978:Receptors, Nicotinic