Prenatal ethanol exposure reduces spinal cord motoneuron number in the fetal rat but does not affect GDNF target tissue protein

Fetal rats were exposed throughout gestation to one of three diets: an etha nol-containing liquid diet, a liquid diet with the isocaloric substitution of sucrose for ethanol or a laboratory chow control diet. At postnatal day 1 (P1), the spinal cords were taken for analyses of motoneuron number and s ize. These analyses revealed a significant loss of motoneurons and a reduct ion of motoneuron size in the ethanol-exposed animals, compared to both suc rose and chow controls. Spinal cord length and ventral horn volume were not altered as a result of ethanol treatment, so the change in motoneuron numb er cannot: be attributed to volumetric changes. The content of the motoneur on survival factor glial cell-line-derived neurotrophic factor (GDNF) was a lso assessed in the P1 limb motoneuron target tissue. This analysis was und ertaken because GDNF is a potent survival factor for developing motoneurons and has been shown to protect this population from ethanol neurotoxicity. Thus, its depletion could contribute to motoneuron loss. These analyses, us ing the ELISA assay, did nor detect reductions in GDNF in the ethanol-expos ed animals. Therefore, alterations in other neurotrophic factors or ethanol neurotoxicity by other means appear to be responsible for the motoneuron l oss. These results are consistent with earlier studies in the chick embryo, which also found reduced motoneuron numbers as a function of developmental ethanol exposure, and point again to the general lethality of ethanol to t he developing nervous system. Copyright (C) 2000 S. Karger AG, Basel.