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Evidence for neuroprotective effects of endogenous brain-derived neurotrophic factor after global forebrain ischemia in rats

Larsson, Elin LU ; Nanobashvili, Avtandil LU ; Kokaia, Zaal LU and Lindvall, Olle LU (1999) In Journal of Cerebral Blood Flow and Metabolism 19(11). p.1220-1228
Abstract

The levels of brain-derived neurotrophic factor (BDNF) vary between different forebrain areas and show region-specific changes after cerebral ischemia. The present study explores the possibility that the levels of endogenous BDNF determine the susceptibility to ischemic neuronal death. To block BDNF activity the authors used the TrkB-Fc fusion protein, which was infused intraventriculary in rats during 1 week before and I week after 5 or 30 minutes of global forebrain ischemia. Ischemic damage was quantified in the striatum and hippocampal formation after 1 week of reperfusion using immunocytochemistry and stereological procedures. After the 30-minute insult, there was a significantly lower number of surviving CA4 pyramidal neurons,... (More)

The levels of brain-derived neurotrophic factor (BDNF) vary between different forebrain areas and show region-specific changes after cerebral ischemia. The present study explores the possibility that the levels of endogenous BDNF determine the susceptibility to ischemic neuronal death. To block BDNF activity the authors used the TrkB-Fc fusion protein, which was infused intraventriculary in rats during 1 week before and I week after 5 or 30 minutes of global forebrain ischemia. Ischemic damage was quantified in the striatum and hippocampal formation after 1 week of reperfusion using immunocytochemistry and stereological procedures. After the 30-minute insult, there was a significantly lower number of surviving CA4 pyramidal neurons, neuropeptide Y-immunoreactive dentate hilar neurons, and choline acetyltransferase- and TrkA-positive, cholinergic striatal interneurons in the TrkB-Fc-infused rats as compared to controls. In contrast, the TrkB-Fc treatment did not influence survival of CA1 or CA3 pyramidal neurons or striatal projection neurons. Also, after the mild ischemic insult (5 minutes), neuronal death in the CA 1 region was similar in the TrkB-Fc- treated and control groups. These results indicate that endogenous BDNF can protect certain neuronal populations against ischemic damage. It is conceivable, though, that efficient neuroprotection after brain insults is dependent not only on this factor but on the concerted action of a large number of neurotrophic molecules.

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author
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Brain-derived neurotrophic factor, Cerebral ischemia, Hippocampus, Neuroprotection, Rat, Striatum
in
Journal of Cerebral Blood Flow and Metabolism
volume
19
issue
11
pages
1220 - 1228
publisher
Nature Publishing Group
external identifiers
  • scopus:0033504237
  • pmid:10566968
ISSN
0271-678X
DOI
10.1097/00004647-199911000-00006
language
English
LU publication?
no
id
d4ef4541-4782-486d-acc4-ca5bf476760d
date added to LUP
2019-09-03 17:01:37
date last changed
2020-05-26 05:31:03
@article{d4ef4541-4782-486d-acc4-ca5bf476760d,
  abstract     = {<p>The levels of brain-derived neurotrophic factor (BDNF) vary between different forebrain areas and show region-specific changes after cerebral ischemia. The present study explores the possibility that the levels of endogenous BDNF determine the susceptibility to ischemic neuronal death. To block BDNF activity the authors used the TrkB-Fc fusion protein, which was infused intraventriculary in rats during 1 week before and I week after 5 or 30 minutes of global forebrain ischemia. Ischemic damage was quantified in the striatum and hippocampal formation after 1 week of reperfusion using immunocytochemistry and stereological procedures. After the 30-minute insult, there was a significantly lower number of surviving CA4 pyramidal neurons, neuropeptide Y-immunoreactive dentate hilar neurons, and choline acetyltransferase- and TrkA-positive, cholinergic striatal interneurons in the TrkB-Fc-infused rats as compared to controls. In contrast, the TrkB-Fc treatment did not influence survival of CA1 or CA3 pyramidal neurons or striatal projection neurons. Also, after the mild ischemic insult (5 minutes), neuronal death in the CA 1 region was similar in the TrkB-Fc- treated and control groups. These results indicate that endogenous BDNF can protect certain neuronal populations against ischemic damage. It is conceivable, though, that efficient neuroprotection after brain insults is dependent not only on this factor but on the concerted action of a large number of neurotrophic molecules.</p>},
  author       = {Larsson, Elin and Nanobashvili, Avtandil and Kokaia, Zaal and Lindvall, Olle},
  issn         = {0271-678X},
  language     = {eng},
  month        = {11},
  number       = {11},
  pages        = {1220--1228},
  publisher    = {Nature Publishing Group},
  series       = {Journal of Cerebral Blood Flow and Metabolism},
  title        = {Evidence for neuroprotective effects of endogenous brain-derived neurotrophic factor after global forebrain ischemia in rats},
  url          = {http://dx.doi.org/10.1097/00004647-199911000-00006},
  doi          = {10.1097/00004647-199911000-00006},
  volume       = {19},
  year         = {1999},
}