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However, the molecular mechanisms underlying these changes are still poorly understood. In our previous studies, we found that ethanol treatment of postnatal day 7 (P7) mice significantly enhances the anandamide levels but not the 2\u2010arachidonylglycerol (2\u2010<jats:styled-content style=\"fixed-case\">AG<\/jats:styled-content>) levels and induces widespread neurodegeneration, but the reason for the lack of significant effects of ethanol on the 2\u2010<jats:styled-content style=\"fixed-case\">AG<\/jats:styled-content> level is unknown. In this study, we examined developmental changes in diacylglycerol lipase\u2010\u03b1, \u03b2 (<jats:styled-content style=\"fixed-case\">DAGL<\/jats:styled-content>\u2010\u03b1 and \u03b2) and monoacylglycerol lipase (<jats:styled-content style=\"fixed-case\">MAGL<\/jats:styled-content>). We found that the levels of these proteins were significantly higher in adult brains compared to those detected early in brain development. Next, we examined the influence of P7 ethanol treatment on these enzymes, finding that it differentially altered the <jats:styled-content style=\"fixed-case\">DAGL<\/jats:styled-content>\u2010\u03b1 protein and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> levels but consistently enhanced those of the <jats:styled-content style=\"fixed-case\">DAGL<\/jats:styled-content>\u2010\u03b2. Interestingly, the ethanol treatment enhanced <jats:styled-content style=\"fixed-case\">MAGL<\/jats:styled-content> protein and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> levels. Inhibition of <jats:styled-content style=\"fixed-case\">MAGL<\/jats:styled-content> with <jats:styled-content style=\"fixed-case\">KML<\/jats:styled-content>29 failed to induce neurodegeneration in P7 mice. Collectively, these findings suggest that ethanol significantly activates <jats:styled-content style=\"fixed-case\">DAGL<\/jats:styled-content>\u2010\u03b2 and <jats:styled-content style=\"fixed-case\">MAGL<\/jats:styled-content> in the neonatal brain, resulting in no net change in 2\u2010<jats:styled-content style=\"fixed-case\">AG<\/jats:styled-content> levels.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13120-fig-0008-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\n<\/jats:p><jats:p>The consumption of ethanol by pregnant women may cause neurological abnormalities, affecting learning and memory processes in children, and are collectively described as fetal alcohol spectrum disorders (FASDs). In our study, ethanol treatment of postnatal day 7 (P7) mice significantly enhanced the levels of the developmentally relevant endocannabinoids anandamide (AEA) but not 2\u2010arachidonylglycerol (2\u2010AG), and induced widespread neurodegeneration, yet the reason for the lack of effects of ethanol on the 2\u2010AG level is unknown. Here, the ethanol treatment of P7 mice causes the specific up\u2010regulation of AEA\u2010CB1R signaling over the 2\u2010AG\u2010CB1R pathway by the specific reorganization of the enzymes that synthesize (DAGL\u2010\u03b1\/\u03b2) and degrade (MAGL) 2\u2010AG. This study demonstrates the neuro\u2010regulatory role of 2\u2010AG metabolizing enzymes in ethanol\u2010induced neurodegeneration in neonatal mice.<\/jats:p>","DOI":"10.1111\/jnc.13120","type":"journal-article","created":{"date-parts":[[2015,4,10]],"date-time":"2015-04-10T06:45:42Z","timestamp":1428648342000},"page":"276-287","source":"Crossref","is-referenced-by-count":29,"title":["Postnatal ethanol exposure alters levels of 2\u2010arachidonylglycerol\u2010metabolizing enzymes and pharmacological inhibition of monoacylglycerol lipase does not cause neurodegeneration in neonatal mice"],"prefix":"10.1111","volume":"134","author":[{"given":"Shivakumar","family":"Subbanna","sequence":"first","affiliation":[{"name":"Division of Analytical Psychopharmacology Nathan Kline Institute for Psychiatric Research Orangeburg New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delphine","family":"Psychoyos","sequence":"additional","affiliation":[{"name":"Institute of Biosciences and Technology Texas A&amp;M University Health Science Center Houston Texas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan","family":"Xie","sequence":"additional","affiliation":[{"name":"Division of Analytical Psychopharmacology Nathan Kline Institute for Psychiatric Research Orangeburg New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balapal S.","family":"Basavarajappa","sequence":"additional","affiliation":[{"name":"Division of Analytical Psychopharmacology Nathan Kline Institute for Psychiatric Research Orangeburg New York USA"},{"name":"New York State Psychiatric Institute College of Physicians &amp; Surgeons Columbia University New York New York USA"},{"name":"Department of Psychiatry College of Physicians &amp; Surgeons Columbia University New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,4,30]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncomms5421"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.2174\/138955707781387920"},{"key":"e_1_2_7_4_1","first-page":"31","volume-title":"Frontiers in Protein and Peptide Sciences","author":"Basavarajappa B. 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