First published online November 18, 2003
Journal of Cell Science 116, e2405 (2003)
Copyright © 2003 The Company of Biologists Limited
Greasing the way to neurotransmission
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 
6-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.
Related articles in JCS:
- Long chain polyunsaturated fatty acids are required for efficient neurotransmission in C. elegans
- Giovanni M. Lesa, Mark Palfreyman, David H. Hall, M. Thomas Clandinin, Claudia Rudolph, Erik M. Jorgensen, and Giampietro Schiavo
JCS 2003 116: 4965-4975.
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