Figure 5  Specific Hippocampus and Piriform Cortex Expression of Transgenic GFPGluR-B
(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]).
(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.
(C) Immunoblot detecting endogenous GluR-B and transgenic GFPGluR-B in the hippocampus of three different mice (#1, #2, #3).
(D) Relative quantification from (C) of transgenic GFPGluR-B compared with endogenous GluR-B in the hippocampus.