Exocyst complex is known to function in the exocytosis network, however, the molecular mechanism is unclear yet. Using UV/trimethylpsoralen mutagenesis, the sec-10 (one component of the exocyst complex) knockout mutant of C. elegans was obtained for the first time. The drug sensitive assays revealed clearly that the sec-10 gene affected the neural signal transmission, however, the electrophysiological assay showed the function of the ionotropic receptors in the neuromuscular junctions (NMJs) were unaltered compared with the wild type (WT). Thus it was assumed that the sec-10 gene might not influence the known ionotropic receptors in the NMJs, but some other pathways instead.