Fig. 1
From: A brainstem-central amygdala circuit underlies defensive responses to learned threats
Norepinephrine β-AR activity is required for CS-elicited freezing responses. a Experimental timeline depicting habituation (Day 1), training (0.6 mA or 0.4 mA US) (Day 2), expression test (Day 3) and drug-free test (Day 4) phases. Vertical arrows indicate time of drug (red arrow) or vehicle (blue arrow) injection for each manipulation. b Systemic injection of the β-AR antagonist propranolol (10 mg/kg) reduced baseline (*p = 0.0283) and CS-elicited (***p = 0.0008) freezing levels during the expression test compared with vehicle control animals (left panel), with no effect observed between groups during a drug-free test (center panel). A within-subject comparison of propranolol treatment versus propranolol-free treatment on CS-elicited freezing showed a significant difference for drug treatment (two-way RM ANOVA test, Interaction: F (1, 22) = 15.79, ***p = 0.0006; Time (Drug versus Drug-free) F (1,22) = 1.678, p = 0.2086; Drug versus Vehicle F (1, 22) = 5.021, *p = 0.0355; Sidak MCS, **p < 0.01 between days for propranolol treated animals, n.s. for vehicle-treated animals). c Systemic injection of the specific β2-AR agonist procaterol (300 µg/kg) enhanced CS-elicited freezing during the expression test (n = 8/group; left panel, *p = 0.0200), with no effect during a drug free test (center panel). Within subject analysis showed a main effect of procaterol on CS-elicited freezing between days in both groups (two-way RM ANOVA test, Interaction: F (1, 14) = 3.991, p = 0.0655; Drug: F (1, 14) = 4.786, *p = 0.0462; Time (Drug versus Drug-free), F (1, 14) = 43.73, ****p < 0.0001; Sidak MCS, ****p < 0.0001 between days for procaterol treated animals, *p < 0.05 for vehicle-treated animals). All error bars indicate mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001
