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. Author manuscript; available in PMC: 2017 Oct 1.
Published in final edited form as: Neuropharmacology. 2016 Jun 22;109:293–305. doi: 10.1016/j.neuropharm.2016.06.022

Figure 4.

Figure 4

Early growth response 1 (Egr1) expression profile in ketamine- and saline-treated animals following contextual fear memory reconsolidation test. The analysis of Egr1 mRNA levels by in situ hybridization in several subregions of the medial prefrontal cortex, hippocampus and amygdala (A) revealed a down-regulation of Egr1 in the hippocampal CA1 subregion in ketamine-treated animals when compared to rats injected with saline. Representative pictures of hippocampal Egr1 signal in saline-(top) and ketamine-treated (bottom) rats. Each square denotes the three hippocampal areas quantified. Regression analyses between the extinction index depicted in Fig. 3C and Egr1 signal in the prelimbic cortex (C), infralimbic cortex (D), and CA1 area (E) revealed a small but not significant negative link between Egr1 signal in the CA1 and contextual fear memory extinction. In (A), each individual data point is depicted within column. *p < 0.05. ACC: anterior cingulate cortex, PLC: prelimbic cortex, ILC: infralimbic cortex, CA1: cornu ammonis 1, CA3: cornu ammonis 3, DG: dentate gyrus, BLA: basolateral amygdala, CeA: central amygdala. Data are represented as mean ± SEM.