F1000Prime Recommendation of [Lim WL et al., Cell Tissue Res 2014, 355(2):409-23]

Antenatal exposure to synthetic glucocorticoids (Gc) is a common treatment used in perinatal medicine for improving the survival of preterm infants and to reduce the risk of respiratory distress syndrome. However, either the physiological or the pharmacological effects of Gc on the developing brain are still not clear. Gc are recognized to influence behavioral responses, emotions and cognitive processes and to take part in the neuroendocrine control of body homeostasis. Moreover, Gc have been proposed to also play a role in brain developmental processes, like neurogenesis and synaptic plasticity {1}. Several studies also indicate that Gc may interfere with the hypothalamic-pituitary-gonadal axis by inhibiting the secretion of gonadotropin-releasing hormone (GnRH) and gonadotropins and possibly affecting the migratory activity of GnRH neurons from the olfactory placode to the preoptic area of the hypothalamus {2}. In order to verify whether maternal Gc exposure might alter GnRH neuronal morphology and number in the offspring, the present study aimed to determine the effect of maternal dexamethasone (DEX) exposure on the development of GnRH neurons labeled with enhanced green fluorescent protein (EGFP) driven by GnRH promoter (TG-GnRH) in transgenic intact male and female rats at different postnatal ages. The results indicate that DEX treatment decreases the number and dendritic development of early postnatal GnRH neurons in the organum vasculosom of the lamina terminalis/preoptic area of the hypothalamus in male newborns, suggesting once more that maternal DEX exposure might contribute to the altered reproductive function and behavior observed during adulthood.