Figure 4. Using inducible cre to bypass the critical NMDAR-dependent cell survival.
(A, B) Representative images of newborn GCs in Grin1f/f mice that were infused with rv CAG GFP-t2A-creER and treated with oil (A) or tamoxifen (B). (C) Deletion of the Grin1 gene initiated in 4-week-old newborn GCs did not affect cell survival. (D) Representative images of dendritic processes in the outer molecular layer of rv GFP-t2A-creER-targeted newborn GCs treated with oil and tamoxifen, and of rv GFP-targeted newborn GCs treated with tamoxifen. (E–G) Quantification of total spine density (E), mushroom spine density (F) and mushroom spine percentage (G) in rv GFP-t2A-creER- and rv GFP-targeted newborn GCs (*p < 0.05). Scale bars: 50 µm (A, B) and 5 µm (D).
Figure 4—figure supplement 1. The recombination efficiency of rv CAG GFP-t2A-creER was tested in the ROSA-lacZ mice.
ROSA-lacZ reporter mice received stereotaxic delivery of retrovirus into the DG and subsequently tamoxifen daily for 5 days starting at 2 weeks after virus injection. Reporter gene expression was analyzed at 2 weeks after the first dose of tamoxifen. Insets on the right side represent GFP− and β-gal-expressing cells, respectively. Scale bar: 50 µm.