Lucassen, P. J. and Bosch, O. J. and Jousma, E. and Kroemer, S. A. and Andrew, R. and Seckl, J. R. and Neumann, I. D. (2009) Prenatal stress reduces postnatal neurogenesis in rats selectively bred for high, but not low, anxiety: possible key role of placental 11 beta-hydroxysteroid dehydrogenase type 2. EUROPEAN JOURNAL OF NEUROSCIENCE, 29 (1). pp. 97-103. ISSN 0953-816X,
Full text not available from this repository. (Request a copy)Abstract
Prenatal stress (PS) produces persistent abnormalities in anxiety-related behaviors, stress responsivity, susceptibility to psychopathology and hippocampal changes in adult offspring. The hippocampus shows a remarkable degree of structural plasticity, notably in response to stress and glucocorticoids. We hypothesized that PS would differentially affect hippocampal neurogenesis in rats selectively bred for genetic differences in anxiety-related behaviors and stress responsivity. Pregnant dams of high anxiety-related behavior (HAB) and low anxiety-related behavior (LAB) strains were stressed between days 5 and 20 of pregnancy. The survival of newly generated hippocampal cells was found to be significantly lower in 43-day-old HAB than in LAB male offspring of unstressed pregnancies. PS further reduced newly generated cell numbers only in HAB rats, and this was paralleled by a reduction in doublecortin-positive cell numbers, indicative of reduced neurogenesis. As maternal plasma corticosterone levels during PS were similar in both strains, we examined placental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2), which catalyses rapid inactivation of maternal corticosterone to inert 11-dehydrocorticosterone and thus serves as a physiological 'barrier' to maternal glucocorticoids. PS significantly increased placental 11 beta-HSD2 activity in LAB, but not HAB, rats. We conclude that PS differentially affects the number of surviving newly generated cells and neurogenesis in HAB and LAB rats. The high sensitivity of hippocampal neurogenesis to PS in HAB rats is paralleled by a failure to increase placental 11 beta-HSD2 activity after stress rather than by different maternal corticosterone responses. Hence, stress-induced placental 11 beta-HSD2 expression may be critical in protecting the fetal brain from maternal stress-induced effects on adult neurogenesis.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ADULT HIPPOCAMPAL NEUROGENESIS; ANTAGONIST MIFEPRISTONE NORMALIZES; GENERATED GRANULE CELLS; DENTATE GYRUS; TRAIT ANXIETY; PSYCHOSOCIAL STRESS; MATERNAL-BEHAVIOR; NEUROENDOCRINE RESPONSES; ANIMAL-MODEL; FEMALE RATS; depression; doublecortin; early life; hippocampus; HPA axis |
| Subjects: | 500 Science > 590 Zoological sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Zoologie > Tierphysiologie/Neurobiologie (Prof. Dr. Inga Neumann) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 12 Oct 2020 08:32 |
| Last Modified: | 12 Oct 2020 08:32 |
| URI: | https://pred.uni-regensburg.de/id/eprint/29721 |
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