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The Journal of Neuroscience, February 11, 2009, 29(6):1826-1833; doi:10.1523/JNEUROSCI.3178-08.2009

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Development/Plasticity/Repair
Prolactin Prevents Chronic Stress-Induced Decrease of Adult Hippocampal Neurogenesis and Promotes Neuronal Fate

Luz Torner,^1,3 * Sandra Karg,^1 * Annegret Blume,¹ Mahesh Kandasamy,² Hans-Georg Kuhn,² Jürgen Winkler,^2,4 Ludwig Aigner,^2,5 and Inga D. Neumann¹

¹Department of Behavioral and Molecular Neuroendocrinology, Institute of Zoology and ²Department of Neurology, University of Regensburg, 93053 Regensburg, Germany, ³Centro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Morelia, Michoacán, 58080, México, ⁴Division of Molecular Neurology, University of Erlangen, 91054 Erlangen, Germany, and ⁵Institute for Molecular Regenerative Medicine, Paracelsus Private Medical University Salzburg, 5020 Salzburg, Austria

Correspondence should be addressed to Inga D. Neumann, Institute of Zoology, University of Regensburg, Universitätsstrasse 31, 93053 Regensburg, Germany. Email: inga.neumann{at}biologie.uni-regensburg.de

Chronic exposure to stress results in a reduction of hippocampal neurogenesis and of hippocampal volume. We examined whether prolactin (PRL), a regulator of the stress response and stimulator of neurogenesis in the subventricular zone, influences neurogenesis in the hippocampal dentate gyrus (DG) of chronically stressed adult C57BL/6 male mice. Chronically stressed (4 h daily immobilization for 21 d) or nonstressed mice were treated with either ovine PRL or vehicle between days 1–14. BrdU was injected daily between days 1–7 to evaluate cell survival and fate, or twice on day 21 to evaluate cell proliferation. Hippocampal cell proliferation was unchanged by either stress exposure or PRL at the end of the treatments. In contrast, the number of cells in the DG that incorporated BrdU during the first phase of the experiment and survived to the end of the experiment was decreased in vehicle-treated stressed mice compared with PRL- or vehicle-treated nonstressed control mice. Stressed animals receiving PRL had significantly more BrdU-labeled cells than vehicle-treated stressed mice at this time point. Cell fate analysis revealed a higher percentage of neurons in PRL- compared with vehicle-treated stressed mice. The results demonstrate that PRL protects neurogenesis in the DG of chronically stressed mice and promotes neuronal fate.

Key words: hippocampus; cell survival; proliferation; HPA axis; corticosterone; dentate gyrus

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Received July 8, 2008; revised Nov. 6, 2008; accepted Dec. 17, 2008.

Correspondence should be addressed to Inga D. Neumann, Institute of Zoology, University of Regensburg, Universitätsstrasse 31, 93053 Regensburg, Germany. Email: inga.neumann{at}biologie.uni-regensburg.de

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