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--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.
-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.
