PMC:1255741 / 30601-31685 JSONTXT

{"project":"2_test","denotations":[{"id":"16216087-9377491-84723750","span":{"begin":413,"end":415},"obj":"9377491"},{"id":"T42602","span":{"begin":413,"end":415},"obj":"9377491"}],"text":"Figure 5 Specific Hippocampus and Piriform Cortex Expression of Transgenic GFPGluR-B\n(A) Schematic diagrams depicting forebrain-specific GluR-B deletion as in Figure 2A and itTA-dependent expression of GFPGluR-B and nuclear-localized β-galactosidase (nLacZ) in GluR-BΔFB mice (termed GluR-BRescue). GFPGluR-B and nLacZ are both encoded by TgOCN1, and itTA is controlled by a fusion of the NR2C silencer element [91] and the αCaMKII promoter (termed TgCN12-itTA [92]).\n(B) In coronal brain sections of mice positive for both transgenes (TgCN12-itTA and TgOCN1) β-galactosidase activity (blue, X-gal, counterstain by eosin) is restricted to hippocampal neurons in CA1, DG, and neurons in the piriform cortex. The same neurons show GFPGluR-B expression when analyzed in immunohistochemical sections with an antibody against GFP. Scale bars: 500 μm.\n(C) Immunoblot detecting endogenous GluR-B and transgenic GFPGluR-B in the hippocampus of three different mice (#1, #2, #3).\n(D) Relative quantification from (C) of transgenic GFPGluR-B compared with endogenous GluR-B in the hippocampus."}