{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,11]],"date-time":"2024-07-11T13:54:57Z","timestamp":1720706097617},"reference-count":40,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2002,4,19]],"date-time":"2002-04-19T00:00:00Z","timestamp":1019174400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2002,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The lipid mediators generated by phospholipases A<jats:sub>2<\/jats:sub> (PLA<jats:sub>2<\/jats:sub>), free arachidonic acid (AA), eicosanoids, and platelet\u2010activating factor, modulate neuronal activity; when overproduced, some of them become potent neurotoxins. We have shown, using primary cortical neuron cultures, that glutamate and secretory PLA<jats:sub>2<\/jats:sub> (sPLA<jats:sub>2<\/jats:sub>) from bee venom (bv sPLA<jats:sub>2<\/jats:sub>) and Taipan snake venom (OS2) elicit synergy in inducing neuronal cell death. Low concentrations of sPLA<jats:sub>2<\/jats:sub> are selective ligands of cell\u2010surface sPLA<jats:sub>2<\/jats:sub> receptors. We investigated which neuronal arachidonoyl phospholipids are targeted by glutamate\u2010activated cytosolic calcium\u2010dependent PLA<jats:sub>2<\/jats:sub> (cPLA<jats:sub>2<\/jats:sub>) and by sPLA<jats:sub>2<\/jats:sub>. Treatment of <jats:sup>3<\/jats:sup>H\u2010AA\u2010labeled cortical neurons with mildly toxic concentrations of sPLA<jats:sub>2<\/jats:sub> (25 ng\/ml, 1.78 nM) for 45 min resulted in a two\u2010 to threefold higher loss of <jats:sup>3<\/jats:sup>H\u2010AA from phosphatidylcholine (PC) than from phosphatidylethanolamine (PE) and in minor changes in other phospholipids. A similar profile, although of greater magnitude, was observed 20 hr posttreatment. Glutamate (80 \u03bcM) induced much less mobilization of <jats:sup>3<\/jats:sup>H\u2010AA than did sPLA<jats:sub>2<\/jats:sub> and resulted in a threefold greater degradation of <jats:sup>3<\/jats:sup>H\u2010AA PE than of <jats:sup>3<\/jats:sup>H\u2010AA PC by 20 hr posttreatment. Combining sPLA<jats:sub>2<\/jats:sub> and glutamate resulted in a greater degradation of PC and PE, and the N\u2010methyl\u2010D\u2010aspartate receptor antagonist MK\u2010801 only blocked glutamate effects. Thus, activation of the arachidonate cascade induced by glutamate and sPLA<jats:sub>2<\/jats:sub> under experimental conditions that lead to neuronal cell death involves the hydrolysis of different (perhaps partially overlapping) cellular phospholipid pools. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.10239","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T23:29:46Z","timestamp":1030318186000},"page":"558-567","source":"Crossref","is-referenced-by-count":30,"title":["Glutamate signalling and secretory phospholipase A<sub>2<\/sub> modulate the release of arachidonic acid from neuronal membranes"],"prefix":"10.1002","volume":"68","author":[{"given":"Elena B.","family":"Rodriguez de Turco","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fannie R.","family":"Jackson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark 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