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Suppressed epileptogenesis in BDNF mutant mice

Kokaia, Merab LU ; Ernfors, Patrik; Kokaia, Zaal LU ; Elmer, Eskil LU ; Jaenisch, Rudolf and Lindvall, Olle LU (1995) In Experimental Neurology 133(2). p.215-224
Abstract
Kindling is an animal model of epilepsy in which repeated electrical stimulations lead to progressive and permanent amplification of seizure activity, culminating in generalized convulsions. Each brief period of seizure activity during kindling epileptogenesis causes a marked, transient increase of the synthesis of brain-derived neurotrophic factor (BDNF) in cortical and hippocampal neurons. We find that the development of kindling is markedly suppressed in mice heterozygous for a deletion of the BDNF gene. In contrast, the maintenance of kindling is unaffected. The mutant mice show lower levels of BDNF mRNA in cortical and hippocampal neurons after seizures than do wild-type mice. Hippocampal mossy fiber sprouting is augmented in BDNF... (More)
Kindling is an animal model of epilepsy in which repeated electrical stimulations lead to progressive and permanent amplification of seizure activity, culminating in generalized convulsions. Each brief period of seizure activity during kindling epileptogenesis causes a marked, transient increase of the synthesis of brain-derived neurotrophic factor (BDNF) in cortical and hippocampal neurons. We find that the development of kindling is markedly suppressed in mice heterozygous for a deletion of the BDNF gene. In contrast, the maintenance of kindling is unaffected. The mutant mice show lower levels of BDNF mRNA in cortical and hippocampal neurons after seizures than do wild-type mice. Hippocampal mossy fiber sprouting is augmented in BDNF mutants but there are no other morphological abnormalities. These results show that BDNF plays an important role in establishing hyperexcitability during epileptogenesis, probably by increasing efficacy in stimulated synapses. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Experimental Neurology
volume
133
issue
2
pages
215 - 224
publisher
Academic Press
external identifiers
  • pmid:7649227
  • scopus:0029160413
ISSN
0014-4886
DOI
10.1006/exnr.1995.1024
language
English
LU publication?
yes
id
e2c18cea-7a19-42f4-8f4f-069ff019deb8 (old id 1108973)
date added to LUP
2008-07-25 11:36:39
date last changed
2017-05-21 03:34:04
@article{e2c18cea-7a19-42f4-8f4f-069ff019deb8,
  abstract     = {Kindling is an animal model of epilepsy in which repeated electrical stimulations lead to progressive and permanent amplification of seizure activity, culminating in generalized convulsions. Each brief period of seizure activity during kindling epileptogenesis causes a marked, transient increase of the synthesis of brain-derived neurotrophic factor (BDNF) in cortical and hippocampal neurons. We find that the development of kindling is markedly suppressed in mice heterozygous for a deletion of the BDNF gene. In contrast, the maintenance of kindling is unaffected. The mutant mice show lower levels of BDNF mRNA in cortical and hippocampal neurons after seizures than do wild-type mice. Hippocampal mossy fiber sprouting is augmented in BDNF mutants but there are no other morphological abnormalities. These results show that BDNF plays an important role in establishing hyperexcitability during epileptogenesis, probably by increasing efficacy in stimulated synapses.},
  author       = {Kokaia, Merab and Ernfors, Patrik and Kokaia, Zaal and Elmer, Eskil and Jaenisch, Rudolf and Lindvall, Olle},
  issn         = {0014-4886},
  language     = {eng},
  number       = {2},
  pages        = {215--224},
  publisher    = {Academic Press},
  series       = {Experimental Neurology},
  title        = {Suppressed epileptogenesis in BDNF mutant mice},
  url          = {http://dx.doi.org/10.1006/exnr.1995.1024},
  volume       = {133},
  year         = {1995},
}