ArticleMolecular biology of the cell2007
Acetylcholinesterase mobility and stability at the neuromuscular junction of living mice.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of Natural Products on Neuromuscular Junction.Current neuropharmacology · 2022Review
- Perlecan, A Multi-Functional, Cell-Instructive, Matrix-Stabilizing Proteoglycan With Roles in Tissue Development Has Relevance to Connective Tissue Repair and Regeneration.Frontiers in cell and developmental biology · 2022Review
- Acupotomy Alleviates Energy Crisis at Rat Myofascial Trigger Points.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Bioactivities ofMolecules (Basel, Switzerland) · 2019Article
- Neurally mediated airway constriction in human and other species: a comparative study using precision-cut lung slices (PCLS).PloS one · 2012Article
- Neuregulin/ErbB regulate neuromuscular junction development by phosphorylation of α-dystrobrevin.The Journal of cell biology · 2011Article
- Distinct localization of collagen Q and PRiMA forms of acetylcholinesterase at the neuromuscular junction.Molecular and cellular neurosciences · 2011Article
- Localization of butyrylcholinesterase at the neuromuscular junction of normal and acetylcholinesterase knockout mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010Article
- Destabilization of the dystrophin-glycoprotein complex without functional deficits in alpha-dystrobrevin null muscle.PloS one · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Acetylcholinesterase (AChE) is an enzyme that terminates acetylcholine neurotransmitter function at the synaptic cleft of cholinergic synapses. However, the mechanism by which AChE number and density are maintained at the synaptic cleft is poorly understood. In this work, we used fluorescence recovery after photobleaching, photo-unbinding, and quantitative fluorescence imaging to investigate the surface mobility and stability of AChE at the adult innervated neuromuscular junction of living mice. In wild-type synapses, we found that nonsynaptic (perisynaptic and extrasynaptic) AChEs are mobile and gradually recruited into synaptic sites and that most of the trapped AChEs come from the perijunctional pool. Selective labeling of a subset of synaptic AChEs within the synapse by using sequential unbinding and relabeling with different colors of streptavidin followed by time-lapse imaging showed that synaptic AChEs are nearly immobile. At neuromuscular junctions of mice deficient in alpha-dystrobrevin, a component of the dystrophin glycoprotein complex, we found that the density and distribution of synaptic AChEs are profoundly altered and that the loss rate of AChE significantly increased. These results demonstrate that nonsynaptic AChEs are mobile, whereas synaptic AChEs are more stable, and that alpha-dystrobrevin is important for controlling the density and stability of AChEs at neuromuscular synapses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.