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Transient neonatal elevation in hypothalamic estrogen receptor mRNA in prenatally-stressed male rats
1INSERM U-394, 'Neurobiol ogie Intégrative', Domaine de Carreire, Bordeaux, France.
Insights
Prenatal stress in male rats transiently increases hypothalamic estrogen receptor (ER) mRNA at birth, suggesting impaired brain masculinization due to reduced testosterone or aromatization during development.
Area of Science:
- Neuroendocrinology
- Developmental Neuroscience
- Behavioral Endocrinology
Background:
- Prenatal stress impacts male offspring's brain sexual differentiation and behavior.
- Brain masculinization relies on testosterone, aromatase activity, and estrogen receptor (ER) density during critical perinatal periods.
Purpose of the Study:
- To investigate the effect of prenatal stress on hypothalamic estrogen receptor (ER) messenger RNA (mRNA) expression in male rats during early development.
- To understand the role of ERs in prenatal stress-induced alterations in brain sexual differentiation.
Main Methods:
- Utilized reverse transcription-polymerase chain reaction (RT-PCR) to quantify ER mRNA levels.
- Examined hypothalamic tissue from prenatally stressed and control male rats at postnatal days 3, 12, and 90.
Main Results:
- A significant elevation in hypothalamic ER mRNA was observed in prenatally stressed male rats at postnatal day 3 (P3) compared to controls.
- This difference in ER mRNA expression was transient, with no significant differences noted at P12 or P90 (adult stage).
- The developmental profile of ER mRNA in stressed males at P3 resembled that of female rats.
Conclusions:
- Prenatal stress leads to a temporary upregulation of hypothalamic ER mRNA in male rats during early development.
- This transient change suggests reduced androgen production or aromatization during the perinatal period, potentially impairing brain masculinization.
- Estrogen receptor dynamics are sensitive to prenatal stress, influencing sexual differentiation of the brain.
Abstract:
Prenatal stress in rats has been found to alter the sexual dimorphism of brain structures and the sexual behavior of male offspring, pointing to an impaired masculinization of the brain during the perinatal period of brain sexual differentiation. Masculinization of the brain depends on the presence during this critical period of three main elements: adequate levels of testosterone, aromatase activity (locally converting testosterone to estradiol), and brain estrogen receptor (ER) density. In the present study, we measured by reverse transcription-polymerase chain reaction (RT-PCR) the levels of ER messenger RNA (mRNA) expression in the hypothalamus of either prenatally-stressed or control male 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 developmental stage (P12, 5.39 +/- 0.65 versus 5.39 +/- 0.47) or in adult animals (P90, 6.79 +/- 1.55 versus 7.07 +/- 1.11). This transient elevation of hypothalamic ER mRNA expression resembles the developmental profile of ER mRNA in females. These observations support the idea that androgens play a pivotal role in the demasculinization process, and suggest that testosterone production or aromatization is reduced in prenatally-stressed males during the perinatal period of sexual differentiation, leading to a transient upregulation of unstimulated estrogen receptors.