For proper functioning of the nervous system, it is crucial that neurons find their appropriate partners and build the correct neural connection patterns. Although cell adhesion molecules (CAMs) have been studied for many years as essential players in neural connections, we have yet to unravel the code by which CAMs encode synaptic specificity. We analyzed the effects of mutations in CAM genes on the morphology and synapses of a set of sensory neurons in the C. elegans male tail. B-type ray sensory neurons express ten genes encoding CAMs. We examined the effect on axon trajectory and localization of presynaptic components in viable mutants of nine of these. We found axon trajectory defects in mutants of UNC-40/DCC, SAX-3/ROBO, and FMI-1/Flamingo/Celsr1. In none of the mutants was presence of presynaptic components in axons lost, and in several the level appeared to increase, suggesting possible accumulation. B-type sensory neurons fasciculate with a second type of ray sensory neuron, the A-type, in axon commissures. We found cell non-autonomous effects consistent with each promoting the trajectory of the other. Overall, single and multiple mutants of CAM genes had limited effects on ray neuron trajectories and accumulation of synaptic components.