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Review
. 2007 Aug;102(3):577-86.
doi: 10.1111/j.1471-4159.2007.04558.x. Epub 2007 Apr 2.

Arachidonic acid metabolism in brain physiology and pathology: lessons from genetically altered mouse models

Francesca Bosetti  1
Affiliations
Review

Arachidonic acid metabolism in brain physiology and pathology: lessons from genetically altered mouse models

Francesca Bosetti. J Neurochem. 2007 Aug.

Abstract

The arachidonic acid (AA) cascade involves the release of AA from the membrane phospholipids by a phospholipase A(2), followed by its subsequent metabolism to bioactive prostanoids by cyclooxygenases coupled with terminal synthases. Altered brain AA metabolism has been implicated in neurological, neurodegenerative, and psychiatric disorders. The development of genetically altered mice lacking specific enzymes of the AA cascade has helped to elucidate the individual roles of these enzymes in brain physiology and pathology. The roles of AA and its metabolites in brain physiology, with a particular emphasis on the phospholipase A(2)/cyclooxygenases pathway, are summarized, and the specific phenotypes of genetically altered mice relevant to brain physiology and neurotoxic models are discussed.

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Figures

Figure 1
Figure 1. The arachidonic acid cascade
The AA cascade involves the release of AA from membrane phospholipids by a PLA2, followed by its metabolism to bioactive eicosanoids – prostaglandins, leukotrienes and epoxy fatty acids –through COX, lipoxygenase and cytochrome P450 epoxygenase enzymes, respectively. EETs = epoxyeicosatrienoic acids; HETEs = hydroxyeicosatetraenoic acids; HPETE = hydroxyperoxyeicosatetraenoic acid; LOX = lipoxygenase; PG = prostaglandin; TXA2 = thromboxane A2
See this image and copyright information in PMC

References

    1. Ahmad AS, Saleem S, Ahmad M, Dore S. Prostaglandin EP1 receptor contributes to excitotoxicity and focal ischemic brain damage. Toxicol Sci. 2006;89:265–270. - PubMed
    1. Akaike A, Kaneko S, Tamura Y, Nakata N, Shiomi H, Ushikubi F, Narumiya S. Prostaglandin E2 protects cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity. Brain Res. 1994;663:237–243. - PubMed
    1. Almer G, Guegan C, Teismann P, Naini A, Rosoklija G, Hays AP, Chen C, Przedborski S. Increased expression of the proinflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis. Ann Neurol. 2001;49:176–185. - PubMed
    1. Andreasson KI, Savonenko A, Vidensky S, Goellner JJ, Zhang Y, Shaffer A, Kaufmann WE, Worley PF, Isakson P, Markowska AL. Age-dependent cognitive deficits and neuronal apoptosis in cyclooxygenase-2 transgenic mice. J Neurosci. 2001;21:8198–8209. - PMC - PubMed
    1. Baile CA, Simpson CW, Bean SM, McLaughlin CL, Jacobs HL. Prostaglandins and food intake of rats: a component of energy balance regulation? Physiol Behav. 1973;10:1077–1085. - PubMed

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