Article date: 1987/1/14
PubMed ID: 2881232
Journal name: Neuroscience letters (ISSN: 0304-3940)
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 (alpha-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.
Author List: Westerberg E, Monaghan D T, Cotman C W, Wieloch T
Publication Types: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
Substances mentioned in the article: Receptors, AMPA; Receptors, Drug; Receptors, Glutamate; Receptors, Neurotransmitter; Ibotenic Acid; Aspartic Acid; N-Methylaspartate; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Kainic Acid;
Mesh terms: Animals; Aspartic Acid/analogs & derivatives; Autoradiography; Hippocampus/metabolism; Ibotenic Acid/analogs & derivatives; Ischemic Attack, Transient/metabolism; Kainic Acid/metabolism; N-Methylaspartate; Rats; Receptors, AMPA; Receptors, Drug/metabolism; Receptors, Glutamate; Receptors, Neurotransmitter/metabolism; Time Factors; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;