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. 2016 Aug 4;6:30743. doi: 10.1038/srep30743

Figure 3. The amount of membrane GluN2B within CA1 determines its contribution to memory consolidation.

Figure 3

(A–D) PKA signaling is necessary for the increase in the amount of membrane GluN2B-containing NMDARs after fear conditioning. Immunoblots (A) and quantification analysis (B–D) of the GluN2B and GluN1 subtypes of NMDAR in membrane lysates of CA1 taken from conditioned rats with intra-CA1 infusions of vehicle (veh) versus the PKA inhibitor Rp-cAMPs (Rp) (B) before training, and taken from conditioned rats with intra-CA1 infusion of veh versus the PKA activator 8-Br-cAMPs (8-Br) (C) or sodium orthovanadate (SOV) (D), a protein tyrosine phosphatase inhibitor, before training with a single CS-US (1 CS-US), normalized to context-vehicle or context-control. **p < 0.01, *p < 0.05 vs. controls; #p < 0.05. (E,F) Up-regulating membrane GluN2B expression within CA1, GluN2B is necessary for the consolidation of memory elicited by 1 CS-US. Pre-conditioning infusions of 8-Br-cAMPs (8-Br-ifen) (E) or SOV (SOV-ifen) (F) coupled with post-conditioning infusion of ifenprodil into CA1 impaired the fear memory elicited by 1 CS-US. Top panels indicate the design of the experiments in E and F. **p < 0.01. (G) Inhibiting the up-regulation of membrane GluN2B within CA1, GluN2B is not necessary for the consolidation of memory elicited by 5 CS-US. Pre-conditioning infusion of Rp-cAMPs coupled with post-conditioning infusion of ifenprodil (Rp-ifen) into CA1 had no impact on the fear memory elicited by 5 CS-US. Top panel shows the design of the experiment. (H) A representative coronal section of an infusion site of the co-infusion of SOV with ifenprodil (SOV-Ifen) into CA1 (upper). Reconstruction of infusion sites in the CA1 region (bottom). Open circles: veh-veh; open squares: SOV-Ifen; open triangles: SOV; filled circles: SOV+Ifen.