We studied the control of pharyngeal excitation in Caenorhabditis elegans. By laser ablating subsets of the pharyngeal nervous system, we found that the MC neuron type is necessary and probably sufficient for rapid pharyngeal pumping. Electropharyngeograms showed that MC transmits excitatory postsynaptic potentials, suggesting that MC acts as a neurogenic pacemaker for pharyngeal pumping. Mutations in genes required for acetylcholine (ACh) release and an antagonist of the nicotinic ACh receptor (nAChR) reduced pumping rates, suggesting that a nAChR is required for MC transmission. To identify genes required for MC neurotransmission, we screened for mutations that cause slow pumping but no other defects. Mutations in two genes,
eat-2 and
eat-18, eliminated MC neurotransmission. A gain-of-function
eat-18 mutation,
ad820sd, and a putative loss-of-function
ent-18 mutation,
ad1110, both reduced the excitation of pharyngeal muscle in response to the nAChR agonists nicotine and carbachol, suggesting that
eat-18 is required for the function of a pharyngeal nAChR. Fourteen recessive mutations in
eat-2 fell into five complementation classes. We found allele-specific genetic interactions between
eat-2 and
eat-18 that correlated with complementation classes of
eat-2. We propose that
eat-18 and
eat-2 function in a multisubunit protein complex involved in the function of a pharyngeal nAChR.