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Nat Neurosci. 1999 Sep;2(9):791-7.

One GABA and two acetylcholine receptors function at the C. elegans neuromuscular junction.

Author information

1
Department 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.

PMID:
10461217
PMCID:
PMC2585773
DOI:
10.1038/12160
[Indexed for MEDLINE]
Free PMC Article

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