Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model

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Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model. / Petersén, Asa; Wörtwein, Gitta; Gruber, Susanne H M; Mathé, Aleksander A.

In: Neuroscience Letters, Vol. 436, No. 3, 2008, p. 305-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Petersén, A, Wörtwein, G, Gruber, SHM & Mathé, AA 2008, 'Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model', Neuroscience Letters, vol. 436, no. 3, pp. 305-8. https://doi.org/10.1016/j.neulet.2008.03.035

APA

Petersén, A., Wörtwein, G., Gruber, S. H. M., & Mathé, A. A. (2008). Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model. Neuroscience Letters, 436(3), 305-8. https://doi.org/10.1016/j.neulet.2008.03.035

Vancouver

Petersén A, Wörtwein G, Gruber SHM, Mathé AA. Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model. Neuroscience Letters. 2008;436(3):305-8. https://doi.org/10.1016/j.neulet.2008.03.035

Author

Petersén, Asa ; Wörtwein, Gitta ; Gruber, Susanne H M ; Mathé, Aleksander A. / Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model. In: Neuroscience Letters. 2008 ; Vol. 436, No. 3. pp. 305-8.

Bibtex

@article{ed019ce0eba511ddbf70000ea68e967b,
title = "Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model",
abstract = "Hippocampal neurogenesis is potentially implicated in etiology of depression and as the final common mechanism underlying antidepressant treatments. However, decreased neurogenesis has not been demonstrated in depressed patients and, in animals, reduced cytogenesis was shown in healthy rats exposed to stressors, but, so far, not in models of depression. Here we report that the number of BrdU positive cells in hippocampus was (1) significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to control FRL, (2) increased in both FSL and FRL following maternal separation, (3) reduced by escitalopram treatment in maternally separated animals to the level found in non-separated animals. These results argue against the prevailing hypothesis that adult cytogenesis is reduced in depression and that the common mechanism underlying antidepressant treatments is to increase adult cytogenesis. The results also point to the importance of using a disease model and not healthy animals for testing effects of potential treatments for human depression and suggest other cellular mechanisms of action than those that had previously been proposed for escitalopram.",
author = "Asa Peters{\'e}n and Gitta W{\"o}rtwein and Gruber, {Susanne H M} and Math{\'e}, {Aleksander A}",
note = "Keywords: Analysis of Variance; Animals; Antidepressive Agents, Second-Generation; Bromodeoxyuridine; Cell Proliferation; Citalopram; Depression; Disease Models, Animal; Hippocampus; Maternal Deprivation; Neurons; Rats; Rats, Inbred Strains; Swimming",
year = "2008",
doi = "10.1016/j.neulet.2008.03.035",
language = "English",
volume = "436",
pages = "305--8",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - Escitalopram reduces increased hippocampal cytogenesis in a genetic rat depression model

AU - Petersén, Asa

AU - Wörtwein, Gitta

AU - Gruber, Susanne H M

AU - Mathé, Aleksander A

N1 - Keywords: Analysis of Variance; Animals; Antidepressive Agents, Second-Generation; Bromodeoxyuridine; Cell Proliferation; Citalopram; Depression; Disease Models, Animal; Hippocampus; Maternal Deprivation; Neurons; Rats; Rats, Inbred Strains; Swimming

PY - 2008

Y1 - 2008

N2 - Hippocampal neurogenesis is potentially implicated in etiology of depression and as the final common mechanism underlying antidepressant treatments. However, decreased neurogenesis has not been demonstrated in depressed patients and, in animals, reduced cytogenesis was shown in healthy rats exposed to stressors, but, so far, not in models of depression. Here we report that the number of BrdU positive cells in hippocampus was (1) significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to control FRL, (2) increased in both FSL and FRL following maternal separation, (3) reduced by escitalopram treatment in maternally separated animals to the level found in non-separated animals. These results argue against the prevailing hypothesis that adult cytogenesis is reduced in depression and that the common mechanism underlying antidepressant treatments is to increase adult cytogenesis. The results also point to the importance of using a disease model and not healthy animals for testing effects of potential treatments for human depression and suggest other cellular mechanisms of action than those that had previously been proposed for escitalopram.

AB - Hippocampal neurogenesis is potentially implicated in etiology of depression and as the final common mechanism underlying antidepressant treatments. However, decreased neurogenesis has not been demonstrated in depressed patients and, in animals, reduced cytogenesis was shown in healthy rats exposed to stressors, but, so far, not in models of depression. Here we report that the number of BrdU positive cells in hippocampus was (1) significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to control FRL, (2) increased in both FSL and FRL following maternal separation, (3) reduced by escitalopram treatment in maternally separated animals to the level found in non-separated animals. These results argue against the prevailing hypothesis that adult cytogenesis is reduced in depression and that the common mechanism underlying antidepressant treatments is to increase adult cytogenesis. The results also point to the importance of using a disease model and not healthy animals for testing effects of potential treatments for human depression and suggest other cellular mechanisms of action than those that had previously been proposed for escitalopram.

U2 - 10.1016/j.neulet.2008.03.035

DO - 10.1016/j.neulet.2008.03.035

M3 - Journal article

C2 - 18406530

VL - 436

SP - 305

EP - 308

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -

ID: 9939190