Key result
Acetylcholine receptor clusters that appear at developing endplates in mammalian muscle arise in part from the redistribution of pre-existing, diffusely distributed receptors.
This preclinical study demonstrates that acetylcholine receptor clusters at developing mammalian endplates form through the redistribution of previously uniformly distributed receptors.
Receptor redistribution shapes mammalian neuromuscular development; leaves open translation to human junction disorders or therapies.
The mechanism of formation of acetylcholine receptor (AChR) clusters at developing mammalian endplates was investigated in vitro, using intercostal muscles from embryonic rats. The muscles were explanted in organ culture with the spinal cord attached, as described previously (Ziskind-Conhaim, L., and M. J. Dennis (1981) Dev. Biol. 85: 243-251). AChRs on the myofibers were labeled with [125I]-alpha-bungarotoxin shortly before clusters appeared and subsequently were cultured in unlabeled toxin for 1 day. Autoradiography of the cultured fibers demonstrated the presence of labeled clusters of AChRs indicating that the AChRs in the newly formed clusters arise from AChRs that had previously been uniformly distributed on the muscle surface.
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Ziskind‐Conhaim et al. (1984) studied Neuromuscular junction development. Organ culture with [125I]-alpha-bungarotoxin labeling vs. Unlabeled muscles or different labeling protocols was evaluated on Density and distribution of acetylcholine receptors (AChRs). Acetylcholine receptor clusters that appear at developing endplates in mammalian muscle arise in part from the redistribution of pre-existing, diffusely distributed receptors.
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