Arachidonic acid enhancement

Ferretti A, Nelson GJ, Schmidt PC, Kelley DS, Bartolini G, and Flanagan VP, Increased dietary arachidonic acid enhances the synthesis of vasoactive eicosanoids in humans. Lipids, Apr 1997 32(4) 435-439. 

Interest in the PGs has recently reverted to their precursor arachidonic acid (AA), which seems to be able to act intracellulary as a second messenger, and also extra-cellularly. In this latter mode it may play a part in LTP. It is known that AA produces a long-lasting enhancement of synaptic transmission in the hippocampus that resembles LTP and in fact activation of NMDA receptors leads to the release of AA by phospholipase A2 (see Dumuis et al. 1988) and inhibition of this enzyme prevents the induction of LTP. AA has also been shown to block the uptake of glutamate (see Williams and Bliss 1989) which would potentiate its effects on NMDA receptors. This would not only prolong LTP but also cause neurotoxicity. 

Shanker G, Mutkus LA, Walker SJ, Aschner M. 2002. Methylmercury enhances arachidonic acid release and cytosolic phospholipase A2 expression in primary cultures of neonatal astrocytes. Brain Res Mol Brain Res 106 1-11. 

Williams J. H., Errington M. L., Lynch M. A., and Bliss T. V. P. (1989). Arachidonic acid induces a long-term activity dependent enhancement of synaptic transmission in the hippocampus. Nature 341 739-742. 

Coffey ET, Sihra TS, Nicholls DG (1993) Protein kinase C and the regulation of glutamate exocytosis from cerebrocortical synaptosomes. J Biol Chem 268 21060-5 Coffey ET, Herrero I, Sihra TS et al (1994a) Glutamate exocytosis and MARCKS phosphorylation are enhanced by a metabotropic glutamate receptor coupled to a protein kinase C synergistically activated by diacylglycerol and arachidonic acid [published erratum appears in J Neurochem 1995 Jan 64(1) 471], J Neurochem 63 1303-10... 

Neuroinflammation emerges as a driving force in chronic neurodegenerative processes like Alzheimer s (AD) or Parkinson s disease (PD). Neuroinflammatoiy mediators such as cytokines, reactive oxygen species and molecules of the arachidonic acid pathway are generated and released by microglia, astrocytes and neurons upon stimulation and activation. In general, enhanced release of these substances has been considered to be detrimental. 

Linoleic acid has been shown to enhance the proliferation of mouse mammary epithelial cells by metabolism to arachidonic acid, which is a precursor of prostaglandin E2 (Bandyopadhyay et al., 1987). However, the mechanism of growth promotion of the unsaturated fatty acids in culture may be related to their importance in the synthesis of cellular membranes (Rintoul et al., 1978 Rockwell et al., 1980), which may have a significant effect on membrane fluidity (Calder et al., 1994). 

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