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Intraventricular Infusion of TrkB-Fc Fusion Protein Promotes Ischemia-Induced Neurogenesis in Adult Rat Dentate Gyrus.

Gustafsson, Elin; Lindvall, Olle LU and Kokaia, Zaal LU (2003) In Stroke: a journal of cerebral circulation 34(11). p.2710-2715
Abstract
Background and Purpose-We have previously shown that delivery of brain-derived neurotrophic factor (BDNF) through direct intrahippocampal gene transduction with a viral vector suppresses the formation of new dentate granule cells triggered by global forebrain ischemia. Here, we investigated whether inhibition of endogenous BDNF alters ischemia-induced neurogenesis in the dentate gyrus. Methods-Rats were subjected to 30 minutes of global forebrain ischemia and then received intraventricular infusion of either the BDNF scavenger, TrkB-Fc fusion protein, or control Hu-Fc for 2 weeks. In parallel, all animals were injected intraperitoneally with the mitosis marker 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU). Animals were killed at 2 or 6... (More)
Background and Purpose-We have previously shown that delivery of brain-derived neurotrophic factor (BDNF) through direct intrahippocampal gene transduction with a viral vector suppresses the formation of new dentate granule cells triggered by global forebrain ischemia. Here, we investigated whether inhibition of endogenous BDNF alters ischemia-induced neurogenesis in the dentate gyrus. Methods-Rats were subjected to 30 minutes of global forebrain ischemia and then received intraventricular infusion of either the BDNF scavenger, TrkB-Fc fusion protein, or control Hu-Fc for 2 weeks. In parallel, all animals were injected intraperitoneally with the mitosis marker 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU). Animals were killed at 2 or 6 weeks after the ischemic insult, and neurogenesis was then assessed immunocytochemically with epifluorescence or confocal microscopy. Results-Infusion of TrkB-Fc fusion protein gave rise to elevated numbers of ischemia-generated new neurons, double-labeled with BrdU and the early neuronal marker Hu or the mature neuronal marker NeuN, in the dentate subgranular zone and granule cell layer at 2 and 6 weeks after the insult. Conclusions-Our findings provide evidence that endogenous BDNF counteracts neuronal differentiation, but not cell proliferation or survival, in ischemia-induced dentate gyrus neurogenesis. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
global, hippocampus, cerebral ischemia, rats, stroke, neurons, brain-derived neurotrophic factor
in
Stroke: a journal of cerebral circulation
volume
34
issue
11
pages
2710 - 2715
publisher
American Heart Association
external identifiers
  • pmid:14563966
  • wos:000186398800037
  • scopus:0242694048
ISSN
1524-4628
DOI
10.1161/01.STR.0000096025.35225.36
language
English
LU publication?
yes
id
449643e1-40e9-403c-ae08-33d982412fdf (old id 118246)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14563966&dopt=Abstract
date added to LUP
2007-07-06 09:25:47
date last changed
2018-01-07 09:23:37
@article{449643e1-40e9-403c-ae08-33d982412fdf,
  abstract     = {Background and Purpose-We have previously shown that delivery of brain-derived neurotrophic factor (BDNF) through direct intrahippocampal gene transduction with a viral vector suppresses the formation of new dentate granule cells triggered by global forebrain ischemia. Here, we investigated whether inhibition of endogenous BDNF alters ischemia-induced neurogenesis in the dentate gyrus. Methods-Rats were subjected to 30 minutes of global forebrain ischemia and then received intraventricular infusion of either the BDNF scavenger, TrkB-Fc fusion protein, or control Hu-Fc for 2 weeks. In parallel, all animals were injected intraperitoneally with the mitosis marker 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU). Animals were killed at 2 or 6 weeks after the ischemic insult, and neurogenesis was then assessed immunocytochemically with epifluorescence or confocal microscopy. Results-Infusion of TrkB-Fc fusion protein gave rise to elevated numbers of ischemia-generated new neurons, double-labeled with BrdU and the early neuronal marker Hu or the mature neuronal marker NeuN, in the dentate subgranular zone and granule cell layer at 2 and 6 weeks after the insult. Conclusions-Our findings provide evidence that endogenous BDNF counteracts neuronal differentiation, but not cell proliferation or survival, in ischemia-induced dentate gyrus neurogenesis.},
  author       = {Gustafsson, Elin and Lindvall, Olle and Kokaia, Zaal},
  issn         = {1524-4628},
  keyword      = {global,hippocampus,cerebral ischemia,rats,stroke,neurons,brain-derived neurotrophic factor},
  language     = {eng},
  number       = {11},
  pages        = {2710--2715},
  publisher    = {American Heart Association},
  series       = { Stroke: a journal of cerebral circulation},
  title        = {Intraventricular Infusion of TrkB-Fc Fusion Protein Promotes Ischemia-Induced Neurogenesis in Adult Rat Dentate Gyrus.},
  url          = {http://dx.doi.org/10.1161/01.STR.0000096025.35225.36},
  volume       = {34},
  year         = {2003},
}