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Development of MK-801, kainate, AMPA, and muscimol bindings sites and the effect of dark rearing in rat visual cortex

We used quantitative autoradiography to determine whether the development of glutamate receptors correlates with the plastic period for monocular deprivation in rat visual cortex. To study glutamate receptors, we incubated sections of rat visual cortex with tritiated (+)-5-methyl-10,11-dihydro-5H-di...

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Bibliographic Details
Published in:Journal of comparative neurology (1911) 1997-06, Vol.383 (1), p.73-81
Main Authors: Gordon, B, Kinch, G, Kato, N, Keele, C, Lissman, T, Fu, L N
Format: Article
Language:English
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Summary:We used quantitative autoradiography to determine whether the development of glutamate receptors correlates with the plastic period for monocular deprivation in rat visual cortex. To study glutamate receptors, we incubated sections of rat visual cortex with tritiated (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10imine maleate (MK-801), tritiated kainate, and tritiated amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA). [ super(3)H]MK-801 is a noncompetitive ligand for the N-methyl-D-aspartate (NMDA) receptor. [ super(3)H]kainate and [ super(3)H]AMPA are competitive ligands for non-NMDA receptors. To compare glutamate binding sites with a nonglutamate binding site, we studied [ super(3)H]muscimol, which binds to gamma -aminobutyric acid (GABA) sub(A) receptors. [ super(3)H]MK-801 binding was maximal at postnatal day 26 (P26) and decreased in adulthood. [ super(3)H]AMPA binding was maximal at P18. [ super(3)H]kainate binding and [ super(3)H]muscimol binding were not age dependent. Dark rearing partially prevented the age-dependent decrease in [ super(3)H]MK-801 binding but had no effect on [ super(3)H]kainate or [ super(3)H]AMPA binding. Dark rearing decreased muscimol binding in adult animals. These results suggest that NMDA receptors, but not other glutamate receptors or GABA sub(A) receptors, are likely to be critical for developmental plasticity in rat visual cortex.
ISSN:0021-9967