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-B^ΔFB mice (termed GluR-B^Rescue). ^GFPGluR-B and nLacZ are both encoded by Tg^OCN1, and itTA is controlled by a fusion of the NR2C silencer element [91] and the αCaMKII promoter (termed Tg^CN12-itTA [92]).

(B) In coronal brain sections of mice positive for both transgenes (Tg^CN12-itTA and Tg^OCN1) 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.