TRANSIENT NEONATAL ELEVATION IN HYPOTHALAMIC ESTROGEN-RECEPTOR MESSENGER-RNA IN PRENATALLY-STRESSED MALE-RATS

Prenatal stress in rats has been found to alter the sexual dimorphism of brain structures and the sexual behavior of male offspring, pointin g to an impaired masculinization of the brain during the perinatal per iod of brain sexual differentiation. Masculinization of the brain depe nds on the presence during this critical period of three main elements : adequate levels of testosterone, aromatase activity (locally convert ing testosterone to estradiol), and brain estrogen receptor (ER) densi ty. In the present study, we measured by reverse transcription-polymer ase chain reaction (RT-PCR) the levels of ER messenger RNA (mRNA) expr ession in the hypothalamus of either prenatally-stressed or control ma le rats at postnatal (P) days 3, 12 and 90. During the early postnatal period (P3), hypothalamic ER mRNA expression was higher in prenatally stressed male rats (6.12 +/- 0.37) than in controls (4.51 +/- 0.55) ( P = 0.015). This difference was not, however, found at a later develop mental stage (P12, 5.39 +/- 0.65 versus 5.39 +/- 0.47) or in adult ani mals (P90, 6.79 +/- 1.55 versus 7.07 +/- 1.11). This transient elevati on of hypothalamic ER mRNA expression resembles the developmental prof ile of ER mRNA in females. These observations support the idea that an drogens play a pivotal role in the demasculinization process, and sugg est that testosterone production or aromatization is reduced in prenat ally-stressed males during the perinatal period of sexual differentiat ion, leading to a transient upregulation of unstimulated estrogen rece ptors.