Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Increased production of the TrkB protein tyrosine kinase receptor after brain insults

Merlio, J P ; Ernfors, P ; Kokaia, Z LU orcid ; Middlemas, D S ; Bengzon, J LU ; Kokaia, M LU ; Smith, M L LU ; Siesjö, B K LU ; Hunter, T and Lindvall, O LU , et al. (1993) In Neuron 10(2). p.64-151
Abstract

The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB mRNA and protein showed the same... (More)

The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB mRNA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.

(Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and , et al. (More)
; ; ; ; ; ; ; ; ; and (Less)
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Animals, Base Sequence, Brain Diseases/metabolism, Brain Ischemia/metabolism, Brain-Derived Neurotrophic Factor, Coma/etiology, Gene Expression, Hippocampus/metabolism, Humans, Hypoglycemia/complications, Kindling, Neurologic, Male, Membrane Glycoproteins/genetics, Membrane Proteins/biosynthesis, Molecular Sequence Data, Nerve Tissue Proteins/metabolism, Protein-Tyrosine Kinases/biosynthesis, RNA, Messenger/metabolism, Rats, Rats, Sprague-Dawley, Rats, Wistar, Receptor, Ciliary Neurotrophic Factor, Receptor, trkC, Receptors, Nerve Growth Factor/genetics, Seizures/physiopathology
in
Neuron
volume
10
issue
2
pages
14 pages
publisher
Cell Press
external identifiers
  • pmid:8439408
  • scopus:0027465479
ISSN
0896-6273
DOI
10.1016/0896-6273(93)90307-D
language
English
LU publication?
no
id
17d74a2f-862c-4679-ba07-ff62239b1a05
date added to LUP
2019-06-25 10:43:00
date last changed
2024-04-02 10:15:33
@article{17d74a2f-862c-4679-ba07-ff62239b1a05,
  abstract     = {{<p>The protein-tyrosine kinases Trk, TrkB, and TrkC are signal-transducing receptors for a family of neurotrophic factors known as the neurotrophins. Here we show that seizures induced by hippocampal kindling lead to a rapid, transient increase of trkB mRNA and protein in the hippocampus. TrkB is a component of a high affinity receptor for brain-derived neurotrophic factor (BDNF). No change was detected in mRNAs for Trk or TrkC, components of the high affinity nerve growth factor or neurotrophin-3 receptors, respectively. trkB mRNA was also transiently increased in the dentate gyrus following cerebral ischemia and hypoglycemic coma; these treatments had no effect on trk and trkC mRNAs. The increase in trkB mRNA and protein showed the same time course and distribution as the increase in BDNF mRNA. These data suggest that BDNF and its receptor may play a local role within the hippocampus in kindling-associated neural plasticity and in neuronal protection following epileptic, ischemic, and hypoglycemic insults.</p>}},
  author       = {{Merlio, J P and Ernfors, P and Kokaia, Z and Middlemas, D S and Bengzon, J and Kokaia, M and Smith, M L and Siesjö, B K and Hunter, T and Lindvall, O and Persson, Håkan}},
  issn         = {{0896-6273}},
  keywords     = {{Animals; Base Sequence; Brain Diseases/metabolism; Brain Ischemia/metabolism; Brain-Derived Neurotrophic Factor; Coma/etiology; Gene Expression; Hippocampus/metabolism; Humans; Hypoglycemia/complications; Kindling, Neurologic; Male; Membrane Glycoproteins/genetics; Membrane Proteins/biosynthesis; Molecular Sequence Data; Nerve Tissue Proteins/metabolism; Protein-Tyrosine Kinases/biosynthesis; RNA, Messenger/metabolism; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptor, Ciliary Neurotrophic Factor; Receptor, trkC; Receptors, Nerve Growth Factor/genetics; Seizures/physiopathology}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{64--151}},
  publisher    = {{Cell Press}},
  series       = {{Neuron}},
  title        = {{Increased production of the TrkB protein tyrosine kinase receptor after brain insults}},
  url          = {{http://dx.doi.org/10.1016/0896-6273(93)90307-D}},
  doi          = {{10.1016/0896-6273(93)90307-D}},
  volume       = {{10}},
  year         = {{1993}},
}