Bosetti Francesca
Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
J Neurochem. 2007 Aug;102(3):577-86. doi: 10.1111/j.1471-4159.2007.04558.x. Epub 2007 Apr 2.
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.
花生四烯酸（AA）级联反应涉及磷脂酶A(2)从膜磷脂中释放出AA，随后AA通过环氧化酶与末端合酶进一步代谢为生物活性前列腺素。大脑AA代谢改变与神经、神经退行性和精神疾病有关。缺乏AA级联反应特定酶的基因改造小鼠的开发，有助于阐明这些酶在大脑生理和病理中的各自作用。本文总结了AA及其代谢产物在大脑生理中的作用，特别强调了磷脂酶A(2)/环氧化酶途径，并讨论了与大脑生理和神经毒性模型相关的基因改造小鼠的特定表型。
