Pathfinding and synapse formation in a zebrafish mutant lacking functional acetylcholine receptors.

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

Neuron

journal_title

Neuron

authors

Westerfield M,Liu DW,Kimmel CB,Walker C

doi

10.1016/0896-6273(90)90139-7

subject

Has Abstract

pub_date

1990-06-01 00:00:00

pages

867-74

issue

6

eissn

0896-6273

issn

1097-4199

pii

0896-6273(90)90139-7

journal_volume

4

pub_type

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