Unlike in wild-type (WT) littermates, spatial firing of hippocampal neurons was completely dissociated from a distinct visual cue and instead, tended to stay constant relative to the recording room in Bax-KO mice. Behaviorally, whereas spatial learning was intact in conventional spatial reference memory tasks, Bax-KO mice were impaired in finding a target location

based on visual landmarks when target locations predicted by dead reckoning and visual landmarks were made incongruent. These results provide converging evidence for the role of DG in binding animal’s internal spatial map with the sensory information on external landmarks in GSK621 ic50 building a distinct spatial representation for each environment.”
“FE65 is expressed predominantly in the brain and interacts with the C-terminal domain

of beta-amyloid precursor protein (APP). We examined hippocampus-dependent memory and in vivo long-term potentiation (LTP) at the CA1 synapses with isoform-specific FE65 knockout (p97FE65(-/-)) mice. When examined using the Morris water maze, p97FE65(-/-) mice were impaired for the hidden platform task but showed normal performance in the probe test. To further discriminate the role of FE65 in acquisition and memory consolidation, we examined p97FE65(-/-) mice with temporal dissociative passive avoidance (TDPA) and contextual fear conditioning (CFC). p97FE65(-/-) learn more mice showed impaired short-term memory for both TDPA and CFC when tested 10 min after training. After multiple TDPA training sessions, the crossover latency of some p97FE65(-/-) mice reached the cutoff value, but it significantly decayed in 8 d. At the Schaffer collateral-CA1 synapses, p97FE65(-/-) mice showed defective early-phase LTP (E-LTP). These results demonstrate novel roles of FE65 in synaptic plasticity, acquisition, and retention for certain forms of memory formation.”
“Reactivation can destabilize

previously consolidated memories, rendering them vulnerable to disruption and necessitating a process of reconsolidation in order for them to be maintained. Quizartinib concentration This process of destabilization and reconsolidation has commonly been cited as a means by which established memories can be updated or modified. However, little direct evidence exists to support this view. The present study addressed this issue by analyzing the influence of novel salient information present at the time of memory reactivation on the likelihood of the reactivated memory to become destabilized and vulnerable to disruption. Rats explored sample objects and, some time later, received systemic injections of the N-methyl-D-aspartic acid (NMDA) receptor antagonist MK-801 or saline prior to memory reactivation. When object memories were relatively young or weakly encoded, MK-801 significantly disrupted reconsolidation regardless of the reactivation conditions.