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Prolactin prevents chronic stress-induced decrease of adult hippocampal neurogenesis and promotes neuronal fate.

Artikel i vetenskaplig tidskrift
Författare Luz Torner
Sandra Karg
Annegret Blume
Mahesh Kandasamy
Hans-Georg Kuhn
Jürgen Winkler
Ludwig Aigner
Inga D Neumann
Publicerad i The Journal of neuroscience : the official journal of the Society for Neuroscience
Volym 29
Nummer/häfte 6
Sidor 1826-33
ISSN 1529-2401
Publiceringsår 2009
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 1826-33
Språk en
Länkar dx.doi.org/10.1523/JNEUROSCI.3178-0...
Ämnesord Animals, Cell Differentiation, physiology, Cell Proliferation, Chronic Disease, Dentate Gyrus, cytology, physiology, Growth Inhibitors, physiology, Male, Mice, Mice, Inbred C57BL, Neurogenesis, physiology, Neurons, cytology, Prolactin, physiology, therapeutic use, Sheep, Stress, Psychological, metabolism, pathology, prevention & control
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

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.

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