{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T05:49:30Z","timestamp":1791179370229,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,3,29]],"date-time":"2013-03-29T00:00:00Z","timestamp":1364515200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp; Exp Res"],"published-print":{"date-parts":[[2013,8]]},"abstract":"Background<\/jats:title>We have previously shown that ethanol (E<\/jats:styled-content>tOH<\/jats:styled-content>) increases cellular apoptosis to developing neurons via the effects on oxidative stress of neurons directly and via increasing production of microglia\u2010derived factors. To study further the mechanism ofE<\/jats:styled-content>tOH<\/jats:styled-content>action on neuronal apoptosis, we determined the effects of 2 well\u2010knownPKA<\/jats:styled-content>activators, dibutyryl cAMP<\/jats:styled-content>(dbcAMP<\/jats:styled-content>) and brain\u2010derived neurotrophic factor (BDNF<\/jats:styled-content>), onE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010activated oxidative stress and apoptotic processes in the hypothalamic neurons in the presence and absence of microglial cells' influence.<\/jats:p><\/jats:sec>Methods<\/jats:title>In enriched neuronal cells from fetal rat hypothalami treated withE<\/jats:styled-content>tOH<\/jats:styled-content>or with conditioned medium fromE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010treated microglia, we measured cellular apoptosis by the free nucleosome assay and the levels of cAMP<\/jats:styled-content>,BDNF<\/jats:styled-content>,O<\/jats:roman><\/jats:styled-content>2\u2212<\/jats:sup>, reactive oxygen species (ROS<\/jats:styled-content>), nitrite, glutathione (GSH<\/jats:styled-content>), and catalase following treatment withE<\/jats:styled-content>tOH<\/jats:styled-content>orE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010treated microglial culture conditioned medium. Additionally, we tested the effectiveness of dbcAMP<\/jats:styled-content>andBDNF<\/jats:styled-content>in preventingE<\/jats:styled-content>tOH<\/jats:styled-content>orE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010treated microglial conditioned medium on cellular apoptosis and oxidative stress in enriched hypothalamic neuronal cell in primary cultures.<\/jats:p><\/jats:sec>Results<\/jats:title>Neuronal cell cultures following treatment withE<\/jats:styled-content>tOH<\/jats:styled-content>orE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010activated microglial conditioned medium showed decreased production levels of cAMP<\/jats:styled-content>andBDNF<\/jats:styled-content>. EtOH also increased apoptotic death as well as oxidative status, as demonstrated by higher cellular levels of oxidants but lower levels of antioxidants, in neuronal cells. These effects ofE<\/jats:styled-content>tOH<\/jats:styled-content>on oxidative stress and cell death were enhanced by the presence of microglia. Treatment withBDNF<\/jats:styled-content>or dbcAMP<\/jats:styled-content>decreasedE<\/jats:styled-content>tOH<\/jats:styled-content>orE<\/jats:styled-content>tOH<\/jats:styled-content>\u2010activated microglial conditioned medium\u2010induced changes in the levels of intracellular free radicals,ROS<\/jats:styled-content>andO<\/jats:roman><\/jats:styled-content>2\u2212<\/jats:sup>, nitrite,GSH<\/jats:styled-content>, and catalase.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>These data support the possibility thatE<\/jats:styled-content>tOH<\/jats:styled-content>by acting directly and via increasing the production of microglial\u2010derived factors reduces cellular levels ofcAMP<\/jats:styled-content>andBDNF<\/jats:styled-content>to increase cellular oxidative status and apoptosis in hypothalamic neuronal cells in primary cultures.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12104","type":"journal-article","created":{"date-parts":[[2013,3,29]],"date-time":"2013-03-29T15:14:22Z","timestamp":1364570062000},"page":"1370-1379","source":"Crossref","is-referenced-by-count":65,"title":["Cyclic Adenosine Monophosphate and Brain\u2010Derived Neurotrophic Factor Decreased Oxidative Stress and Apoptosis in Developing Hypothalamic Neuronal Cells: Role of Microglia"],"prefix":"10.1111","volume":"37","author":[{"given":"Nadka I.","family":"Boyadjieva","sequence":"first","affiliation":[{"name":"Endocrine Program Department of Animal Sciences Graduate Program of Neuroscience Rutgers, The State University of New Jersey New Brunswick New Jersey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dipak K.","family":"Sarkar","sequence":"additional","affiliation":[{"name":"Endocrine Program Department of Animal Sciences Graduate Program of Neuroscience Rutgers, The State University of New Jersey New Brunswick 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