Neuron
ArticleMotor nerve terminal loss from degenerating muscle fibers
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Early differences in membrane properties at the neuromuscular junctions of ALS model mice: Effects of 25-hydroxycholesterol
2021, Life SciencesCitation Excerpt :Increase in number of end plate islets (fragmentation) occurs with aging and has also been observed early in mouse models of muscular dystrophy [66,67] as well as in SOD-G37R mice [68]. Furthermore, fragmentation can be induced by crush- or laser-induced muscle fiber damage [69,70]. In ALS patients, fragmentation of postsynaptic apparatus is present at early disease stage [8].
Alterations of neuromuscular junctions in Duchenne muscular dystrophy
2020, Neuroscience LettersCitation Excerpt :Some studies report strong evidence showing that disrupted NMJ morphology is the consequence of muscle fiber degeneration and regeneration [37,50,51,59], but others have suggested that NMJ fragmentation in mdx muscle is independent of degeneration and regeneration [3,46]. In support of the latter, NMJ post-synaptic morphology, including AChR area, is normal in fibers of muscle subjected to toxin-induced degeneration [75,88]. It is thought that the motor neuron in DMD and mdx mice is unaffected, except for axonal sprouting near the NMJ and changes in the terminal bouton.
Pre- and post-synaptic roles of action potential activity in synapse elimination revealed by using ectopic neuromuscular junction formation by a foreign nerve
2020, Neuroscience LettersCitation Excerpt :Some possibilities for the causal factors of these post-synaptic events are discussed in [49]. It is also important to note that depletion of post-synaptic AChRs was initially described as the earliest event in developmental synapse elimination, followed by withdrawal of the overlying nerve terminals [1,46]: it was later demonstrated, however, that this is only a rare occurrence, because normally the AChR clusters are vacated by the withdrawing terminals and taken over by the winners in the competition [55]. The focus of the second group of reviewed experiments is the timing of the action potentials carried by the multiple reinnervating axons that converge on each and the same AChR aggregate.
Glial cell line-derived neurotrophic factor (GDNF) expression and NMJ plasticity in skeletal muscle following endurance exercise
2014, NeuroscienceCitation Excerpt :Sarcopenia appears to be fiber-type specific as large motor units that innervate fast-twitch skeletal muscle present as the most vulnerable to denervation, followed by intermediate and finally the most resilient small motor units (Frey et al., 2000; Doherty, 2003; Edström et al., 2007). The denervation of large motor units causes terminal sprouting of adjacent surviving motor units to muscle fibers left without innervation (Rich and Lichtman, 1989). This increases the size of the remaining motor units and may cause overburdening and exhaustion of that neuron, progressively leading to further denervation and eventual disability and mortality.
Long-term reinnervation effects after sciatic nerve lesions in adult rats
2005, Annals of AnatomyNeuregulin inhibits acetylcholine receptor aggregation in myotubes
2004, Journal of Biological ChemistryCitation Excerpt :First, spontaneous AChR clusters are very scarce extrajunctionally in innervated muscle, but become more common following denervation (34). Second, during synapse elimination at the developing NMJ, in the absence of synaptic takeover, the postsynaptic apparatus appears to be lost underneath the axon terminal prior to its retraction (10–12). AChRs remain stabilized when the vacated synaptic site is reoccupied by the remaining axon, whereas a rapid loss of AChRs occurs when synaptic sites are not reoccupied (35).