ZFIN ID: ZDB-PUB-961014-1246
Pathfinding and synapse formation in a zebrafish mutant lacking functional acetylcholine receptors
Westerfield, M., Liu, D.W., Kimmel, C.B., and Walker, C.
Date: 1990
Source: Neuron   4: 867-874 (Journal)
Registered Authors: Kimmel, Charles B., Liu, Dennis, Walker, Charline, Westerfield, Monte
Keywords: none
MeSH Terms:
  • Animals
  • Antibodies, Monoclonal
  • Axons/physiology
  • Bungarotoxins/metabolism
  • Cyprinidae/genetics*
  • Electric Stimulation
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/physiology
  • Genes, Lethal
  • Genes, Recessive
  • Macromolecular Substances
  • Membrane Potentials
  • Microscopy, Electron
  • Motor Neurons/physiology
  • Motor Neurons/ultrastructure
  • Muscles/physiology
  • Muscles/ultrastructure
  • Mutation*
  • Neuromuscular Junction/physiology
  • Neuromuscular Junction/ultrastructure
  • Receptors, Cholinergic/genetics*
  • Receptors, Cholinergic/metabolism
  • Synapses/physiology*
  • Zebrafish/genetics*
PubMed: 2361010 Full text @ Neuron
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.