Alcohol exposure during pregnancy causes fetal alcohol spectrum disorder in the offspring characterized by various neural developmental deficits, growth retardation and facial abnormalities. A common endophenotype of fetal alcohol exposed offspring is an elevated neuroendocrine response of the HPA axis [1]–[3], particularly an increase in circulating ACTH and corticosterone, which has been suggested to be due, at least in part, to the deleterious effects of alcohol exposure on hypothalamic β-endorphin producing neurons [4], [5]. During the stress response, hypothalamic peptides are released through several signaling cascades, such as the release of corticotropin-releasing hormone (CRH) followed by the release of various POMC-derived peptides. POMC is a relatively large peptide that is cleaved into multiple biologically active subunits, including β-endorphin and α-melanocyte stimulating hormone (α-MSH). Upon stimulation, β-endorphin synthesis, primarily within the arcuate nucleus of the hypothalamus, is activated by CRH release from terminals emerging from the paraventricular nucleus (PVN) of the hypothalamus, which is in turn inhibited by β-endorphin release [3], [6]. POMC-derived neuropeptides play a vital role in many other processes such as energy homeostasis, stress response, immune functions and
