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