Nortriptyline mediates behavioral effects without affecting hippocampal cytogenesis in a genetic rat depression model.
(2009) In Neuroscience Letters 451. p.148-151- Abstract
- A prevailing hypothesis is that neurogenesis is reduced in depression and that the common mechanism for antidepressant treatments is to increase it in adult hippocampus. Reduced neurogenesis has been shown in healthy rats exposed to stress, but it has not yet been demonstrated in depressed patients. Emerging studies now indicate that selective serotonin reuptake inhibitors can, exert behavioral effects without affecting neurogenesis in mice. Here we extend our previous findings demonstrating that the number of BrdU positive cells in hippocampus was significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to the control strain the Flinders Resistant Line (FRL). We also show that chronic treatment with... (More)
- A prevailing hypothesis is that neurogenesis is reduced in depression and that the common mechanism for antidepressant treatments is to increase it in adult hippocampus. Reduced neurogenesis has been shown in healthy rats exposed to stress, but it has not yet been demonstrated in depressed patients. Emerging studies now indicate that selective serotonin reuptake inhibitors can, exert behavioral effects without affecting neurogenesis in mice. Here we extend our previous findings demonstrating that the number of BrdU positive cells in hippocampus was significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to the control strain the Flinders Resistant Line (FRL). We also show that chronic treatment with the tricyclic antidepressant nortriptyline exerts behavioral effects in the Porsolt forced swim test without affecting hippocampal cell proliferation in the FSL model. These results strengthen the arguments against hypothesis of neurogenesis being necessary in etiology of depression and as requisite for effects of antidepressants, and illustrate the importance of using a disease model and not healthy animals to assess effects of potential therapies for major depressive disorder. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1289817
- author
- Petersén, Åsa LU ; Wörtwein, Gitta ; Gruber, Susanne H M ; El-Khoury, Aram and Mathé, Aleksander A
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Neuroscience Letters
- volume
- 451
- pages
- 148 - 151
- publisher
- Elsevier
- external identifiers
-
- wos:000263583000011
- pmid:19135130
- scopus:58949093384
- pmid:19135130
- ISSN
- 0304-3940
- DOI
- 10.1016/j.neulet.2008.12.046
- language
- English
- LU publication?
- yes
- id
- ca46acb0-9f38-4077-967c-8e5c855beea2 (old id 1289817)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19135130?dopt=Abstract
- date added to LUP
- 2016-04-04 07:27:01
- date last changed
- 2022-01-29 02:11:16
@article{ca46acb0-9f38-4077-967c-8e5c855beea2,
abstract = {{A prevailing hypothesis is that neurogenesis is reduced in depression and that the common mechanism for antidepressant treatments is to increase it in adult hippocampus. Reduced neurogenesis has been shown in healthy rats exposed to stress, but it has not yet been demonstrated in depressed patients. Emerging studies now indicate that selective serotonin reuptake inhibitors can, exert behavioral effects without affecting neurogenesis in mice. Here we extend our previous findings demonstrating that the number of BrdU positive cells in hippocampus was significantly higher in a rat model of depression, the Flinders Sensitive Line (FSL) compared to the control strain the Flinders Resistant Line (FRL). We also show that chronic treatment with the tricyclic antidepressant nortriptyline exerts behavioral effects in the Porsolt forced swim test without affecting hippocampal cell proliferation in the FSL model. These results strengthen the arguments against hypothesis of neurogenesis being necessary in etiology of depression and as requisite for effects of antidepressants, and illustrate the importance of using a disease model and not healthy animals to assess effects of potential therapies for major depressive disorder.}},
author = {{Petersén, Åsa and Wörtwein, Gitta and Gruber, Susanne H M and El-Khoury, Aram and Mathé, Aleksander A}},
issn = {{0304-3940}},
language = {{eng}},
pages = {{148--151}},
publisher = {{Elsevier}},
series = {{Neuroscience Letters}},
title = {{Nortriptyline mediates behavioral effects without affecting hippocampal cytogenesis in a genetic rat depression model.}},
url = {{http://dx.doi.org/10.1016/j.neulet.2008.12.046}},
doi = {{10.1016/j.neulet.2008.12.046}},
volume = {{451}},
year = {{2009}},
}