Excitatory amino acid receptors and ischemic brain damage in the rat
(1987) In Neuroscience Letters 73(2). p.119-124- Abstract
The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [3H]AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no... (More)
The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [3H]AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no change was noted in the N-methyl-d-aspartate or kainic acid binding sites over this time period.
(Less)
- author
- Westerberg, Eva ; Monaghan, Daniel T. ; Cotman, Carl W. and Wieloch, Tadeusz LU
- organization
- publishing date
- 1987-01-14
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain damage, Glutamate receptor, Hippocampus, Ischemia
- in
- Neuroscience Letters
- volume
- 73
- issue
- 2
- pages
- 6 pages
- publisher
- Elsevier
- external identifiers
-
- pmid:2881232
- scopus:0023089706
- ISSN
- 0304-3940
- DOI
- 10.1016/0304-3940(87)90004-8
- language
- English
- LU publication?
- yes
- id
- 8da9e001-cd6d-47c4-b5e6-d5b8b40a370f
- date added to LUP
- 2019-06-13 17:40:47
- date last changed
- 2024-01-01 10:30:37
@article{8da9e001-cd6d-47c4-b5e6-d5b8b40a370f, abstract = {{<p>The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA<sub>1</sub> hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [<sup>3</sup>H]AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no change was noted in the N-methyl-d-aspartate or kainic acid binding sites over this time period.</p>}}, author = {{Westerberg, Eva and Monaghan, Daniel T. and Cotman, Carl W. and Wieloch, Tadeusz}}, issn = {{0304-3940}}, keywords = {{Brain damage; Glutamate receptor; Hippocampus; Ischemia}}, language = {{eng}}, month = {{01}}, number = {{2}}, pages = {{119--124}}, publisher = {{Elsevier}}, series = {{Neuroscience Letters}}, title = {{Excitatory amino acid receptors and ischemic brain damage in the rat}}, url = {{http://dx.doi.org/10.1016/0304-3940(87)90004-8}}, doi = {{10.1016/0304-3940(87)90004-8}}, volume = {{73}}, year = {{1987}}, }