Journal:

Article Title: Remodeling of ?-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit composition in hippocampal neurons after global ischemia

doi:

Figure Lengend Snippet: Global ischemia induces cell-specific suppression of GluR2, but not GluR1, immunolabeling in CA1 pyramidal neurons. GluR2 (Upper) and GluR1 (Lower) immunolabeling in the CA1 pyramidal cell layer (A–D), the CA3a pyramidal cell layer (E–H) and DG granule cell layer (I–L) in sections from a control animal (A, C, E, G, I, and K) and an experimental animal 72 h after ischemia (B, D, F, H, J, and L). Data are typical of two control and four ischemic animals. Ischemia induced down-regulation of GluR2, but not GluR1, in CA1 pyramidal neurons. Ischemia did not alter GluR1 or GluR2 immunolabeling in CA3a pyramidal neurons or DG granule cells. so: stratum oriens; sp: stratum pyramidale; sr: stratum radiatum; slu: stratum lucidum; ml: molecular layer; gcl: granule cell layer; h: hilus.

Article Snippet: Sections then were incubated with fluorescein avidin DCS (GluR2) or Texas red avidin D (GluR1; Vector Laboratories), dry-mounted, and cover-slipped with Vectashield to reduce quenching.

Techniques: Immunolabeling

Journal:

Article Title: Remodeling of ?-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit composition in hippocampal neurons after global ischemia

doi:

Figure Lengend Snippet: Global ischemia induces subunit-specific down-regulation of GluR2 abundance in CA1. (A) Microdissection of the hippocampus for Western blot analysis. (B) Representative Western blots probed with GluR2C Ab (Upper) and relative GluR2 subunit abundance (defined as the ratio of band densities for experimental vs. control samples; Lower) for CA1 (Left) and CA3-DG (Right) in control and postischemic animals. Protein samples of hippocampal CA1 and CA3-DG were from control animals at 72 h and experimental animals at 48, 60, and 72 h after brief (5 min) global ischemia. Relative GluR2 subunit abundance was markedly decreased in CA1 at 60 h (to 61.5 ± 11.9% of control; n = 6 per time point; P < 0.05) and 72 h after ischemia (to 57.6 ± 7.9% of control, P < 0.05; n = 6 per time point). GluR2 subunit abundance was unchanged in CA3-DG. (C) Western blots probed with GluR1C Ab (Upper) and relative GluR1 subunit abundance displayed as in B. Aliquots of the same protein samples (hippocampal CA1 and CA3-DG) used in B were run on different gels. GluR1 subunit abundance was not altered in the CA1 or CA3-DG at any times examined after ischemia (n = 6 per time point). Band densities were corrected for protein concentration. Bars are means ± SEMs. Asterisks indicate significant difference from control values (P < 0.05).

Article Snippet: Sections then were incubated with fluorescein avidin DCS (GluR2) or Texas red avidin D (GluR1; Vector Laboratories), dry-mounted, and cover-slipped with Vectashield to reduce quenching.

Techniques: Laser Capture Microdissection, Western Blot, Protein Concentration