(A,B) BLA of Fosf/f mice were infected with viruses expressing Cre-GFP (B) or GFP alone (A). C-FOS induction was tested 10 days later, 4 hr after onset of seizures in response to kainic acid (20 mg/kg). Cre injected BLA’s had reduced C-FOS expression confirming penetrance of the knock-out. (C–E) Fos deletion from BLApn attenuates CTA learning. Fos f/f mice received Cre and control viruses bilaterally and were trained for CTA 10 days later and then tested after an additional 48 hr. (C) Both groups exhibited significant memory reflected by reduced saccharin consumption between training and testing sessions. Mixed ANOVA revealed a significant effect of training (F(1,14) = 154.6, p=5.9×10−9), but not of knockout (F(1,14) = 0.15, p=0.70), although there was a significant interaction (F(1,14) = 9.67, p=0.008). Post-hoc analysis revealed that both GFP (N = 8) and Cre (N = 8) group reductions following CTA (test vs. train) were significant (GFP: p=9×10−6; Cre: p=3.6×10−4) but differences between the other conditions were not (CTA-GFP vs CTA-Cre: p=0.26 and test-GFP vs test-Cre: p=0.065). (D) Fos deletion from BLApn reduced memory strength measured as the fraction of saccharin consumed (test/training): 25% (GFP) versus 49% (Cre) and this difference in ratios was significant (t(14)=-2.7; p=0.017). (E) Reduced saccharin consumption cannot be attributed to overall inhibition of drinking as the amount of water drunk 8 hr later did not differ (p=0.26). *p<0.05; **p<0.01. See also Figure 3—source datas 1 and 2.
Figure 3—source data 1. Saccharin consumption (ml) during CTA training and test.
Figure 3—source data 2. Fraction of saccharin consumed (Test/Training).