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These effects are manifested in <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> neurons by a decrease in <jats:italic>Pomc<\/jats:italic> gene expression, a decrement in the levels of its derived peptide <jats:italic>\u03b2<\/jats:italic>\u2010endorphin and a dysregulation of the stress response in the adult offspring. The <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content> axis is a major neuroendocrine system with pivotal physiological functions and mode of regulation. This system has been shown to be perturbed by prenatal alcohol exposure. It has been demonstrated that the perturbation of the <jats:styled-content style=\"fixed-case\">HPA<\/jats:styled-content> axis by <jats:styled-content style=\"fixed-case\">FAE<\/jats:styled-content> is long\u2010lasting and is linked to molecular, neurophysiological, and behavioral changes in exposed individuals. Recently, we showed that the dysregulation of the <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> system function by <jats:styled-content style=\"fixed-case\">FAE<\/jats:styled-content> is induced by epigenetic mechanisms such as hypermethylation of <jats:italic>Pomc<\/jats:italic> gene promoter and an alteration in histone marks in <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> neurons. This developmental programming of the <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> system by <jats:styled-content style=\"fixed-case\">FAE<\/jats:styled-content> altered the transcriptome in <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> neurons and induced a hyperresponse to stress in adulthood. These long\u2010lasting epigenetic changes influenced subsequent generations via the male germline. We also demonstrated that the epigenetic programming of the <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> system by <jats:styled-content style=\"fixed-case\">FAE<\/jats:styled-content> was reversed in adulthood with the application of the inhibitors of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> methylation or histone modifications. Thus, prenatal environmental influences, such as alcohol exposure, could epigenetically modulate <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> neuronal circuits and function to shape adult behavioral patterns. Identifying specific epigenetic factors in hypothalamic <jats:styled-content style=\"fixed-case\">POMC<\/jats:styled-content> neurons that are modulated by fetal alcohol and target <jats:italic>Pomc<\/jats:italic> gene could be potentially useful for the development of new therapeutic approaches to treat stress\u2010related diseases in patients with fetal alcohol spectrum disorders.<\/jats:p>","DOI":"10.1111\/acer.12497","type":"journal-article","created":{"date-parts":[[2014,7,28]],"date-time":"2014-07-28T17:40:07Z","timestamp":1406569207000},"page":"2323-2330","source":"Crossref","is-referenced-by-count":26,"title":["Fetal Alcohol Programming of Hypothalamic Proopiomelanocortin System by Epigenetic Mechanisms and Later Life Vulnerability to Stress"],"prefix":"10.1111","volume":"38","author":[{"given":"Rola","family":"Bekdash","sequence":"first","affiliation":[{"name":"Endocrinology Program Department of Animal Sciences, Rutgers The State University of New Jersey New Brunswick New 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