Abstract:
:We induced and characterized a recessive lethal mutation, nic-1, in zebrafish that blocks the function of muscle acetylcholine (ACh) receptors. Homozygous nic-1 embryos are nonmotile and fail to respond to exogenous application of cholinergic agonists, although their muscles contract in response to direct electrical stimulation. Moreover, we do not detect cell surface labeling by alpha-bungarotoxin or monoclonal antibodies that recognize the other three subunits of ACh receptors. Motoneurons, however, establish morphologically normal patterns of innervation and normal neuromuscular junctions. We suggest that neither transmitter-mediated nerve signaling nor any other aspect of ACh receptor function is required for the formation of appropriate nerve connections in this system.
journal_name
Neuronjournal_title
Neuronauthors
Westerfield M,Liu DW,Kimmel CB,Walker Cdoi
10.1016/0896-6273(90)90139-7subject
Has Abstractpub_date
1990-06-01 00:00:00pages
867-74issue
6eissn
0896-6273issn
1097-4199pii
0896-6273(90)90139-7journal_volume
4pub_type
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