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Prenatal stress and neonatal rat brain development
D L A Van den Hove1, H W M Steinbusch, A Scheepens
1Department of Pediatrics, Research Institute Growth and Development, Faculty of Medicine, Maastricht University, P. Debyelaan 25, P. O. Box 5800, 6202 AZ, Maastricht, The Netherlands. d.vandenhove@np.unimaas.nl
Insights
Prenatal stress in rats reduced brain cell growth and altered stress hormone levels, increasing vulnerability to mood disorders like depression later in life.
Area of Science:
- Neuroscience
- Developmental Psychology
- Endocrinology
Background:
- Prenatal stress is linked to later-life mood disorders.
- Mechanisms connecting prenatal stress to psychopathology are not fully understood.
Purpose of the Study:
- To investigate the impact of prenatal stress on early postnatal brain development in rats.
- To identify potential biological markers for increased psychopathology risk.
Main Methods:
- Studied fetal growth, corticosterone secretion, cell proliferation, caspase-3 activity, and brain-derived neurotrophic factor (BDNF) in prenatally stressed rats.
- Utilized maternal deprivation and assessed outcomes on postnatal days 1 and 8.
Main Results:
- Prenatal stress slightly reduced birth weight and altered corticosterone levels postnatally.
- Observed a ~50% decrease in brain cell proliferation and increased caspase-3 activity in the hippocampus.
- Found reduced BDNF protein in olfactory bulbs and hippocampus of stressed males.
Conclusions:
- Prenatal stress induces detrimental changes in early brain development.
- These neurobiological alterations may contribute to the heightened susceptibility to mood disorders, including depression.
Abstract:
Chronic or repeated stress during human fetal brain development has been associated with various learning, behavioral, and/or mood disorders, including depression in later life. The mechanisms accounting for these effects of prenatal stress are not fully understood. The aim of this study was to investigate the effects of prenatal stress on early postnatal brain development, a disturbance of which may contribute to this increased vulnerability to psychopathology. We studied the effects of prenatal stress on fetal growth, stress-induced corticosterone secretion, brain cell proliferation, caspase-3-like activity and brain-derived neurotrophic factor protein content in newborn Fischer 344 rats. In addition to a slight reduction in birth weight, prenatal stress was associated with elevated corticosterone levels (33.8%) after 1 h of maternal deprivation on postnatal day 1, whereas by postnatal day 8 this pattern was reversed (-46.5%). Further, prenatal stress resulted in an approximately 50% decrease in brain cell proliferation just after birth in both genders with a concomitant increase in caspase-3-like activity within the hippocampus at postnatal day 1 (36.1%) and at postnatal day 5 (females only; 20.1%). Finally, brain-derived neurotrophic factor protein content was reduced in both the olfactory bulbs (-24.6%) and hippocampus (-28.2%) of prenatally stressed male offspring at postnatal days 1 and 5, respectively. These detrimental central changes observed may partly explain the increased susceptibility of prenatally stressed subjects to mood disorders including depression in later life.

