Several environmental chemicals have the capability of impacting endocrine function (endocrine disrupting chemicals [EDCs]), and therefore they may have long-term consequences, especially if exposure occurs during embryonic development. In this study we present data relative to two widely used animal models: the Japanese quail and the mouse. These two species have been used to understand neural, neuroendocrine, and behavioral components of reproduction and are optimal models to understand how these components are altered by precocious exposure to EDCs. In particular, we discuss the effects of embryonic exposure to diethylstilbestrol, genistein, or ethylene,1,1-dichloro-2,2-bis(p-chlorophenyl) on the sexually dimorphic parvocellular vasotocin system and male copulatory behavior in quail and the effects of bisphenol A on the nitrinergic and kisspeptin systems and their behavioral impact in the mouse. In both models the exposure to EDCs during the critical period (early embryonic period in birds, perinatal period in rodents) alters the differentiation of relevant sexually dimorphic pathways, often inducing the appearance of a sex-reversed neurochemical phenotype that is the most probable cause of the final alteration of sexually differentiated behaviors in the adult animal. In conclusion, the data presented here should stimulate a critical reanalysis of the way to determine the "safe" exposure levels to EDCs for wild species and humans, considering behavior and related neural circuits among the factors to be analyzed.