Although the membranes of neuronal cells contain precisely controlled amounts of long-chain polyunsaturated fatty acids (LC-PUFAs) and defects in LC-PUFA metabolism are associated with some human neuronal pathologies, exactly how LC-PUFAs are involved in neuronal function is unknown. On p. 4965, Giovanni Lesa et al. remedy this by showing that in C. elegans LC-PUFAs are essential for efficient neurotransmission. In C. elegans, a single Δ6-desaturase enzyme, encoded by fat3, is essential for LC-PUFA synthesis. fat3 mutant worms have movement and egg-laying defects indicative of neuronal impairment. These defects are functional rather than developmental since treating adult mutant worms with LC-PUFAs rescues the phenotype. Because fat3 mutants release very low amounts of neurotransmitters and have fewer synaptic vesicles than do wild-type worms, the researchers conclude that there are insufficient synaptic vesicles to support normal neurotransmission in these mutants. Additional experiments are now needed to reveal how a LC-PUFA deficit affects synaptic vesicle numbers.