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Differential inhibition of neurogenesis and angiogenesis by corticosterone in rats stimulated with electroconvulsive seizures

Ekstrand, Joakim LU ; Hellsten, Johan LU ; Wennström, Malin LU and Tingström, Anders LU (2008) In Progress in Neuro-Psychopharmacology and Biological Psychiatry 32(6). p.1466-1472
Abstract
Antidepressant drugs and electroconvulsive seizure (ECS)-treatment, an animal model of electroconvulsive therapy, induce neurogenesis in adult rats. Stress and high levels of corticosterone (CORT) on the contrary inhibit neurogenesis. Hippocampal neurogenesis has been described to occur in an angiogenic niche where proliferation of neural progenitors takes place in an environment with active vascular growth. Here we investigate the effect of ECS-treatment on the proliferation of endothelial cells and neuronal precursors in hippocampus of CORT-treated rats. Bromodeoxyuridine (BrdU) was used to identify dividing cells. The number of newborn neuronal precursors and endothelial cells was quantified in the subgranular zone (SGZ) and the... (More)
Antidepressant drugs and electroconvulsive seizure (ECS)-treatment, an animal model of electroconvulsive therapy, induce neurogenesis in adult rats. Stress and high levels of corticosterone (CORT) on the contrary inhibit neurogenesis. Hippocampal neurogenesis has been described to occur in an angiogenic niche where proliferation of neural progenitors takes place in an environment with active vascular growth. Here we investigate the effect of ECS-treatment on the proliferation of endothelial cells and neuronal precursors in hippocampus of CORT-treated rats. Bromodeoxyuridine (BrdU) was used to identify dividing cells. The number of newborn neuronal precursors and endothelial cells was quantified in the subgranular zone (SGZ) and the molecular layer (ML) of the dentate gyrus. The increase in neuronal precursor proliferation in the SGZ following ECS-treatment was not inhibited by elevated levels of CORT despite CORT strongly inhibiting ECS-induced endothelial cell proliferation. Also in the ML CORT-treatment inhibited the ECS-induced angiogenic response. We conclude that despite common factors regulating neurogenesis and angiogenesis, ECS-induced proliferation of neuronal precursors can take place even if the angiogenic response is blunted. Whether inhibition of angiogenesis affects other steps in the chain of events leading to the formation of fully integrated granule neurons remains to be elucidated. (C) 2008 Elsevier Inc. All rights reserved. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
neurogenesis, hippocampus, electroconvulsive seizures, angiogenesis, depression
in
Progress in Neuro-Psychopharmacology and Biological Psychiatry
volume
32
issue
6
pages
1466 - 1472
publisher
Elsevier
external identifiers
  • wos:000258819200015
  • scopus:47749156367
  • pmid:18583010
ISSN
0278-5846
DOI
10.1016/j.pnpbp.2008.05.012
language
English
LU publication?
yes
id
a9c011a6-52fe-4e8c-b36b-27a0c4b11865 (old id 1247353)
date added to LUP
2016-04-01 12:09:32
date last changed
2022-03-21 00:17:30
@article{a9c011a6-52fe-4e8c-b36b-27a0c4b11865,
  abstract     = {{Antidepressant drugs and electroconvulsive seizure (ECS)-treatment, an animal model of electroconvulsive therapy, induce neurogenesis in adult rats. Stress and high levels of corticosterone (CORT) on the contrary inhibit neurogenesis. Hippocampal neurogenesis has been described to occur in an angiogenic niche where proliferation of neural progenitors takes place in an environment with active vascular growth. Here we investigate the effect of ECS-treatment on the proliferation of endothelial cells and neuronal precursors in hippocampus of CORT-treated rats. Bromodeoxyuridine (BrdU) was used to identify dividing cells. The number of newborn neuronal precursors and endothelial cells was quantified in the subgranular zone (SGZ) and the molecular layer (ML) of the dentate gyrus. The increase in neuronal precursor proliferation in the SGZ following ECS-treatment was not inhibited by elevated levels of CORT despite CORT strongly inhibiting ECS-induced endothelial cell proliferation. Also in the ML CORT-treatment inhibited the ECS-induced angiogenic response. We conclude that despite common factors regulating neurogenesis and angiogenesis, ECS-induced proliferation of neuronal precursors can take place even if the angiogenic response is blunted. Whether inhibition of angiogenesis affects other steps in the chain of events leading to the formation of fully integrated granule neurons remains to be elucidated. (C) 2008 Elsevier Inc. All rights reserved.}},
  author       = {{Ekstrand, Joakim and Hellsten, Johan and Wennström, Malin and Tingström, Anders}},
  issn         = {{0278-5846}},
  keywords     = {{neurogenesis; hippocampus; electroconvulsive seizures; angiogenesis; depression}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1466--1472}},
  publisher    = {{Elsevier}},
  series       = {{Progress in Neuro-Psychopharmacology and Biological Psychiatry}},
  title        = {{Differential inhibition of neurogenesis and angiogenesis by corticosterone in rats stimulated with electroconvulsive seizures}},
  url          = {{http://dx.doi.org/10.1016/j.pnpbp.2008.05.012}},
  doi          = {{10.1016/j.pnpbp.2008.05.012}},
  volume       = {{32}},
  year         = {{2008}},
}