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

We describe an electrophysiological preparation of the neuromuscular juncti on of the nematode C. elegans, which adds to its considerable genetic and g enomic resources. Mutant analysis, pharmacology and patch-clamp recording s howed that the body wall muscles of wild-type animals expressed a GABA rece ptor and two acetylcholine receptors. The muscle GABA response was abolishe d in animals lacking the GABA receptor gene unc-49. One acetylcholine recep tor was activated by the nematocide levamisole. This response was eliminate d in mutants lacking either the unc-38 or unc-29 genes, which encode alpha and non-alpha acetylcholine receptor subunits, respectively. The second, pr eviously undescribed, acetylcholine receptor was activated by nicotine, des ensitized rapidly and was selectively blocked by dihydro-beta-erythroidine, thus explaining the residual motility of unc-38 and unc-29 mutants. By rec ording spontaneous endogenous currents and selectively eliminating each of these receptors, we demonstrated that all three receptor types function at neuromuscular synapses.