The defining question of early experience studies concerns the mechanism by which environmental effects occurring in early development are “biologically embedded” and thus sustained into adulthood (ie, so-called “environmental programming” effects). The offspring of high-LG mothers exhibit increased hippocampal GR expression from the exon 17 promoter and dampened HPA responses to stress that persist into adulthood. We propose that the differential epigenomic status of the exon 17 GR promoter in the offspring of high-LG mothers serves as a mechanism for this maternal effect. It is important to note that these findings are restricted to the study of a single promoter of but one gene in one region of the brain. The degree to which such results might generalize to other instances of environmental programming remains to be determined. Moreover, further studies are required to determine how maternal behavior alters the epigenomic status of the exon 17 GR promoter. The developmental timecourse study is critical. Recall that the 5' CpG dinucleotide of the NGFIA consensus sequence of the exon 17 promoter is methylated to the same, elevated level in the newborn
