Effects of in utero ethanol exposure on the development of LHRH neurons in the mouse.

Prenatal ethanol exposure has been shown to result in craniofacial malformations as well as alterations of central nervous system morphology and function. Previous studies have demonstrated that acute ethanol exposure on gestational day 7 in the developing C57BL/6J mouse resulted in craniofacial abnormalities similar to that of children with fetal alcohol syndrome. We investigated the effect of ethanol on the migration and number of immunoreactive LHRH (irLHRH) neurons in this strain of mouse. Pregnant mice were intubated with 2 doses of a 25% solution of ethanol 4 h apart on gestational day 7 (G7). Control animals were intubated with water. Animals were sacrificed on G14 or G18 and immunocytochemistry was used to identify irLHRH neurons that were visualized by light microscopy. Fetal ethanol administration did not substantially affect the migration of the LHRH neurons from the medial nasal placode into the forebrain on G14 or G18. The total number of irLHRH neurons was not significantly different on G14 in ethanol-exposed animals as compared to the number in control animals. However, the total number of irLHRH neurons on G18 was significantly less (P less than 0.03) in 4 neuroanatomical regions in fetal ethanol-exposed mice compared to those in control mice; the nasal septum, the traverse area superior to the cribriform plate and ventromedial to the olfactory bulbs, the arch area which included the olfactory tubercle, medial septal nuclei and anterior hypothalamus in G18 fetuses, and preoptic area of the brain. Coronal investigation of the number of irLHRH neurons on G18 indicates that the loss of irLHRH neurons occurred predominantly in the medial region of the rostrum and brain.