Skip to main content
. 2019 Mar 15;116(14):7077–7082. doi: 10.1073/pnas.1901513116

Fig. 5.

Fig. 5.

Blockade of BLA noradrenergic activity prevents the effect of GR agonist treatment into the PrL on neuronal activity changes within the aIC and dHPC. Rats were given a 3-min training trial followed by β-adrenoceptor antagonist propranolol (Prop) (0.3 μg in 0.2 μL) or saline (Sal) administration into the left BLA together with the GR agonist RU 28362 (10 ng in 0.5 μL) or vehicle into the ipsilateral PrL. c-Fos immunofluorescence was assessed 1 h later. (A) Numerical density of c-Fos–positive cells within cortical layers II/III of aIC. Data are presented as fold change (mean ± SEM) (n = 6–9 rats/group, two-way ANOVA: RU 28362 F1,26 = 5.10, P = 0.03; propranolol F1,26 = 1.75, P = 0.20; interaction F1,26 = 6.63, P = 0.02). (B) Numerical density of c-Fos–positive cells within the pyramidal cell layer of CA1 (two-way ANOVA: RU 28362 F1,25 = 5.06, P = 0.03; propranolol F1,25 = 0.41, P = 0.53; interaction F1,25 = 2.73, P = 0.11). (C) Numerical density of c-Fos–positive cells within the granule cell layer of dDG (two-way ANOVA: RU 28362 F1,25 = 2.04, P = 0.17; propranolol F1,25 = 0.28, P = 0.60; interaction F1,25 = 0.84, P = 0.37). (D) Numerical density of c-Fos–positive cells within the NRE (two-way ANOVA: RU 28362 F1,26 = 2.32, P = 0.14; propranolol F1,26 = 6.58, P = 0.02; interaction F1,26 = 4.24, P = 0.049). *P < 0.05, **P < 0.01 vs. vehicle; ◆◆P < 0.01 vs. RU 28362 alone.