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Updated: Aug 4, 2026

Paradigms for Pharmacological Characterization of C. elegans Synaptic Transmission Mutants
Published on: August 19, 2008
One GABA and two acetylcholine receptors function at the C. elegans neuromuscular junction
1Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, Utah 84112-0840, USA. richmond@biology.utah.edu
Abstract:
We describe an electrophysiological preparation of the neuromuscular junction of the nematode C. elegans, which adds to its considerable genetic and genomic resources. Mutant analysis, pharmacology and patch-clamp recording showed that the body wall muscles of wild-type animals expressed a GABA receptor and two acetylcholine receptors. The muscle GABA response was abolished in animals lacking the GABA receptor gene unc-49. One acetylcholine receptor was activated by the nematocide levamisole. This response was eliminated in mutants lacking either the unc-38 or unc-29 genes, which encode alpha and non-alpha acetylcholine receptor subunits, respectively. The second, previously undescribed, acetylcholine receptor was activated by nicotine, desensitized rapidly and was selectively blocked by dihydro-beta-erythroidine, thus explaining the residual motility of unc-38 and unc-29 mutants. By recording spontaneous endogenous currents and selectively eliminating each of these receptors, we demonstrated that all three receptor types function at neuromuscular synapses.
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