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Dynamic changes of excitatory amino acid receptors in the rat hippocampus following transient cerebral ischemia

Westerberg, E. ; Monaghan, D. T. ; Kalimo, H. ; Cotman, C. W. and Wieloch, T. W. LU (1989) In The Journal of Neuroscience 9(3). p.798-805
Abstract
The changes in excitatory amino acid receptor ligand binding induced by transient cerebral ischemia were studied in the rat hippocampal subfields. Ten minutes of ischemia was induced by common carotid artery occlusion combined with hypotension, and the animals were allowed variable periods of recovery ranging from 1 day to 4 weeks. The binding of 3H-AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) to quisqualate receptors, 3H-kainic acid (KA) to kainate receptors, and 3H-glutamate to N-methyl-D-aspartate (NMDA) receptors as determined by quantitative autoradiography. One week following ischemia the CA1 region of the hippocampus displayed a severe (90%) dendrosomatic lesion with preservation of presynaptic terminals. This was... (More)
The changes in excitatory amino acid receptor ligand binding induced by transient cerebral ischemia were studied in the rat hippocampal subfields. Ten minutes of ischemia was induced by common carotid artery occlusion combined with hypotension, and the animals were allowed variable periods of recovery ranging from 1 day to 4 weeks. The binding of 3H-AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) to quisqualate receptors, 3H-kainic acid (KA) to kainate receptors, and 3H-glutamate to N-methyl-D-aspartate (NMDA) receptors as determined by quantitative autoradiography. One week following ischemia the CA1 region of the hippocampus displayed a severe (90%) dendrosomatic lesion with preservation of presynaptic terminals. This was associated with a 60% decrease in AMPA binding and a 25% decrease in glutamate binding to NMDA receptors. At 4 weeks postischemia, both AMPA and NMDA sites were greatly reduced. Although the dentate gyrus granule cells are resistant to an ischemic insult of this magnitude, this region showed marked changes in receptor binding. One week following ischemia, the AMPA and NMDA binding decreased by approximately 40 and 20%, respectively. Following 2 weeks of recovery, the NMDA binding was not significantly different from control level, while the AMPA binding remained depressed up to 4 weeks postischemia. The high density of KA binding sites in the inner molecular layer of the dentate gyrus was unaffected by the ischemic insult, despite an extensive degeneration of cells in the hilus of dentate gyrus which projects glutamatergic afferents to this area. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
The Journal of Neuroscience
volume
9
issue
3
pages
8 pages
publisher
Society for Neuroscience
external identifiers
  • pmid:2538582
  • scopus:0024511427
ISSN
0270-6474
DOI
10.1523/JNEUROSCI.09-03-00798.1989
language
English
LU publication?
yes
id
dbf6f65e-d119-42e6-8583-2557f7ea6e33
date added to LUP
2019-06-13 17:34:26
date last changed
2024-01-01 10:28:57
@article{dbf6f65e-d119-42e6-8583-2557f7ea6e33,
  abstract     = {{The changes in excitatory amino acid receptor ligand binding induced by transient cerebral ischemia were studied in the rat hippocampal subfields. Ten minutes of ischemia was induced by common carotid artery occlusion combined with hypotension, and the animals were allowed variable periods of recovery ranging from 1 day to 4 weeks. The binding of 3H-AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) to quisqualate receptors, 3H-kainic acid (KA) to kainate receptors, and 3H-glutamate to N-methyl-D-aspartate (NMDA) receptors as determined by quantitative autoradiography. One week following ischemia the CA1 region of the hippocampus displayed a severe (90%) dendrosomatic lesion with preservation of presynaptic terminals. This was associated with a 60% decrease in AMPA binding and a 25% decrease in glutamate binding to NMDA receptors. At 4 weeks postischemia, both AMPA and NMDA sites were greatly reduced. Although the dentate gyrus granule cells are resistant to an ischemic insult of this magnitude, this region showed marked changes in receptor binding. One week following ischemia, the AMPA and NMDA binding decreased by approximately 40 and 20%, respectively. Following 2 weeks of recovery, the NMDA binding was not significantly different from control level, while the AMPA binding remained depressed up to 4 weeks postischemia. The high density of KA binding sites in the inner molecular layer of the dentate gyrus was unaffected by the ischemic insult, despite an extensive degeneration of cells in the hilus of dentate gyrus which projects glutamatergic afferents to this area.}},
  author       = {{Westerberg, E. and Monaghan, D. T. and Kalimo, H. and Cotman, C. W. and Wieloch, T. W.}},
  issn         = {{0270-6474}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{3}},
  pages        = {{798--805}},
  publisher    = {{Society for Neuroscience}},
  series       = {{The Journal of Neuroscience}},
  title        = {{Dynamic changes of excitatory amino acid receptors in the rat hippocampus following transient cerebral ischemia}},
  url          = {{http://dx.doi.org/10.1523/JNEUROSCI.09-03-00798.1989}},
  doi          = {{10.1523/JNEUROSCI.09-03-00798.1989}},
  volume       = {{9}},
  year         = {{1989}},
}