Figure 4.

GluN2B-NMDARs are required for SDIA extinction memory destabilization. (a) Animals were trained in SDIA (TR; 0.4 mA/2 s) and, beginning 24 h later, they were submitted to one daily extinction training trial for 5 consecutive days. One day after the last extinction training trial, animals received bilateral intra-CA1 infusions of vehicle (VEH; 0.1% DMSO in saline) or the GluN2A-containing NMDAR antagonist TCN201 (TCN; 0.05 µg/side), and 20 min later, SDIA extinction memory was reactivated (RA). Five minutes after RA, rats received bilateral intra-dorsal CA1 infusions of VEH or rapamycin (RAP; 0.02 µg/side), an inhibitor of mammalian target of RAP (mTOR). Retention was assessed 1 day and 7 days later (Test). (b) Animals were treated as in A except that 20 min before RA they received bilateral intra-CA1 infusions of VEH or the GluN2B-containing NMDAR antagonist RO25-6981 (RO; 2.5 µg/side). (c) Animals trained in SDIA received bilateral intra-CA1 infusions of VEH, RO or TCN one day post-training and, 20 min later, were submitted to a SDIA memory retention test. (d) Animals received bilateral intra-dorsal CA1 infusions of VEH, TCN or RO and 20 min later were submitted to a 5 min-long open field arena exploration session to determine locomotor activity. Representative traces show locomotor activity from rats that received VEH, TCN or RO. Data are expressed as median ± IQR or mean ± SEM. (*) p < 0.05, (**) p < 0.01, (***) p < 0.001 versus VEH in Dunn's multiple comparisons after Kruskal–Wallis test; n = 9–13 animals per group.