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First published online November 18, 2003


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Journal of Cell Science 116, e2405 (2003)
Copyright © 2003 The Company of Biologists Limited


In this issue

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 {Delta}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.


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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. [Abstract] [Full Text]  




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