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. 2015 Sep 2;5:13633. doi: 10.1038/srep13633

Figure 4. Memory disruption is dependent on destabilization mediated by GluN2B-containing NMDA receptors in the hippocampus.

Figure 4

(A) Schematic representation of the behavioral procedures: 48 h after training, rats received an intrahippocampal (CA1 area) infusion of ifenprodil (IFEN) or its vehicle (VEH), and, 15 min later, were re-exposed to the fear conditioning context without the US (shock) – the Reactivation session – either with or without the presence of a distractor (DIST); all groups were tested on day 5. (B) Percent of freezing time during Reactivation and Test sessions expressed as mean ± S.E.M. (VEH, N = 9, VEH + DIST, N = 13, IFEN, N = 12, and IFEN + DIST, N = 12). (a) significantly different from its control group, VEH (P < 0.05; Newman-Keuls post-hoc test); (b) significantly different from its control group, VEH (P < 0.05; Newman-Keuls post-hoc test); in both sessions, there is no significant difference among the remaining (unmarked) groups; (c) performance differs significantly between sessions (P < 0.05; Newman-Keuls post-hoc test).