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However, it is not known how glutamatergic insults affect <jats:italic>in vivo<\/jats:italic> endocannabinoid homeostasis, i.e. <jats:italic>N<\/jats:italic>\u2010arachidonoylethanolamine (anandamide) and 2\u2010arachidonoylglycerol (2\u2010AG), as well as other constituents of\u00a0their lipid families, <jats:italic>N<\/jats:italic>\u2010acylethanolamines (NAEs) and 2\u2010monoacylglycerols (2\u2010MAGs), respectively. Here we employed three <jats:italic>in vivo<\/jats:italic> neonatal rat models characterized by widespread neurodegeneration as a consequence of altered glutamatergic neurotransmission and assessed changes in endocannabinoid homeostasis. A 46\u2010fold increase of cortical NAE concentrations (anandamide, 13\u2010fold) was noted 24\u2003h after intracerebral NMDA injection, while less severe insults triggered by mild concussive head trauma or NMDA receptor blockade produced a less pronounced NAE accumulation. By contrast, levels of 2\u2010AG and other 2\u2010MAGs were virtually unaffected by the insults employed, rendering it likely that key enzymes in biosynthetic pathways of the two different endocannabinoid structures are not equally associated to intracellular events that cause neuronal damage <jats:italic>in vivo.<\/jats:italic> Analysis of cannabinoid CB<jats:sub>1<\/jats:sub> receptor mRNA expression and\u00a0binding capacity revealed that cortical subfields exhibited an up\u2010regulation of these parameters following mild concussive head trauma and exposure to NMDA receptor blockade. This may suggest that mild to moderate brain injury may trigger elevated endocannabinoid activity via concomitant increase of anandamide levels, but not 2\u2010AG, and CB<jats:sub>1<\/jats:sub> receptor density.<\/jats:p>","DOI":"10.1046\/j.1471-4159.2001.00542.x","type":"journal-article","created":{"date-parts":[[2003,3,12]],"date-time":"2003-03-12T06:56:36Z","timestamp":1047452196000},"page":"1415-1427","source":"Crossref","is-referenced-by-count":171,"title":["Anandamide, but not 2\u2010arachidonoylglycerol, accumulates during <i>in vivo<\/i> neurodegeneration"],"prefix":"10.1111","volume":"78","author":[{"given":"Henrik H.","family":"Hansen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia C.","family":"Schmid","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"Bittigau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabel","family":"Lastres\u2010Becker","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando","family":"Berrendero","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Manzanares","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chrysanthy","family":"Ikonomidou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harald H. 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