| Reference code: | PT/FB/BL-2012-217.06 |
| Location: | Arquivo PCA - Pasta 27/2012
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Title:
| A role for lipocalin-2 in hippocampal neurogenesis modulation
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| Publication year: | 2015
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URL:
| http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=3a2ee3c5-1f04-47c0-9dc1-97d906996574&cKey=1d74de64-a47b-4a3c-8492-3bc2fc7dfe18&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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| Abstract/Results: | ABSTRACT:
Stress is defined as a challenge to the homeostatic equilibrium of the organism and when long lasting it severely affects quality of life. In fact, stress maladaptation is considered to be an etiological factor in the emergence of mood disorders like 5depression and anxiety. Stress response elicits a cascade of hormonal and behavioral changes as an attempt to maintain homeostasis and at the level of the central nervous system (CNS), the hippocampus is considered to be a central target and executor of adaptative responses. Of interest, the hippocampus is unique in its structural and cellular plasticity, in the sense that, even in adulthood, stem cells reside and continuously give rise to new neurons. This adult neurogenesis is extremely dynamic and modulated by pharmacological, environmental and physiological stimuli and the newborn neurons are considered to highly contribute to the local network. Of interest, adult neurogenesis is well known to be regulated by stress and, conversely, to regulate stress responses. Of course there is no simple, linear relationship between stress hormones and adult neurogenesis. As an attempt to disclose putative factors in this crosstalk of stress modulation, in the present work we have assessed the modulation of hippocampal neurogenesis in an animal model with a targeted deletion of lipocalin-2 (LCN2). As part of the lipocalin protein family, LCN2 plays a critical role in the regulation of various phyisiological processess, such as inflammation and innate immune response. Several roles for cell proliferation and death have also been attributed to this protein, including during development, in hematopoiesis and even cancer, mainly recognized due to the capacity of LCN2 to traffic iron within cells. In addition, LCN2-null mice were described, at a physiological level, to present a sustained activation of the HPA axis translated into increased levels of corticosterone, accompanied by an anxious and depressive-like phenotypes. Also it was described to control anxiety and neuronal excitability upon stress. But specifically how is hippocampal neurogenesis being modulated upon LCN2 deletion and to which extent it contributes to animal's behavior and stress response is not quite known. Here we show that LCN2-null mice exhibit cell proliferation deficits, accompanied by impairments in adult neurogenesis progress and in contextual fear conditioning paradigms. The current observations will certainly contribute to the current interests on the role of hippocampal neurogenesis in the etiology of mood, identifying LCN2 as a possible key regulator of executor of adaptative responses at the hippocampus.
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| Accessibility: | Document doesn't exist in file
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Language:
| eng
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| Collection: | (NEUROGENESIS ) |
| Author: | Morgado, P.
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Secondary author(s):
| Ferreira, A. C., Mesquita, S. D., Novais, A., Neves, S. , Sousa, N., Palha, J., Sousa, J. C., Marques, F.
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Document type:
| Online abstract
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Number of reproductions:
| 1
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Reference:
| Morgado, P., Ferreira, A. C., Mesquita, S. D., Novais, A., Neves, S., Sousa, N., Palha, J., Sousa, J. C., & Marques, F. (2015, November). A role for lipocalin-2 in hippocampal neurogenesis modulation. Paper presented at the Society for Neuroscience (SFN), Chicago, USA. Abstract available at http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=3a2ee3c5-1f04-47c0-9dc1-97d906996574&cKey=1d74de64-a47b-4a3c-8492-3bc2fc7dfe18&mKey=d0ff4555-8574-4fbb-b9d4-04eec8ba0c84
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| Indexed document: | No
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| Keywords: | Neurogenesis / Behavior / Neurosphere
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