Fig. 10

Schematic representation of proposed neuroimmune mechanism underlying the stimulatory effect of maternal ethanol exposure at a moderate dose on early development of MCH neurons and ultimately on the offspring’s behavior. Maternal ethanol exposure (2 g/kg/day, E10–E15) increases CCL2 signaling at its receptor CCR2, which in turn stimulates radial glia progenitor cells with CCL2 in the NEP that function to promote MCH neurogenesis in the NEP and also radial glia processes with CCL2 in the mHYP that facilitate the migration of MCH neurons toward the LH where they themselves colocalize CCL2 and CCR2. These molecular changes in the embryo, consistently stronger females than males, may contribute to the increased alcohol consumption and reward behaviors observed later in adolescent offspring, often more strongly in females. LH, lateral hypothalamus; MCH, melanin-concentrating hormone; mHYP, medial hypothalamus; NEP, neuroepithelium