Cui et al. [20] showed that inducing NMDAR knockout 6 months after formation of contextual or cued fear memories disrupted retention of these remote memories.
Some patients with serious cases could not rid themselves of the memories of fighting SARS, and these memories disrupted their daily activities.
Similar to the αCaMKII+/− heterozygous mutation, the Itgβ2−/− and Soat1−/− mutations may affect physiological processes (i.e. temporal cortex LTP) required for remote memory without disrupting hippocampal-dependent memory formation [3], [7], [34], [35].
136 For example, returning to the experimental question of whether the DLPFC enhances memory targets or suppresses distractors during working memory, 113 disrupting the DLPFC might result in the representation of targets being affected such that the (MVPA-identified) representations are decreased as a result of the disturbance of top-down enhancement.
And now, a new study published in the journal PLOS Computational Biology is shedding light on how stress - the blast of a fire engine's siren, say - interferes with working memory by disrupting PFC neurons' firing patterns.
If one memory task disrupts the other memory task, then the two tasks may use the same working memory system.
Bearing these two facts in mind, we asked whether sulfasalazine during the reconsolidation protocol could induce memory extinction by prolonged NF-κB inhibition during memory reactivation rather than by disrupting memory reconsolidation.
Experiment 1demonstrated that immediate post-training administration of MK-801 produced a consolidation impairment at postnatal day 37. Experiment 2 extended this result, showing that MK-801 administered immediately following memory reactivation disrupted reconsolidation.
Here, we used ketamine to impair spatial working memory and disrupt behavior to examine the capacity for the GABAAα2/3 agonist 7- 1,1-dimethylethyl -6- 2-ethyl-2H-1,2,4-triazol-3-ylmethoxy -3- 2-fluorophenyl -1,2,4-triazolo[4,3-b]pyridazine (TPA023) to reverse these symptoms.
However, only NMDAR-mediated memory was disrupted in GluR2-cKO mice.
Consistent with the suggestion that its effects on synaptic plasticity are relevant to central nervous system function, associative learning and memory is disrupted when NCS-1 is absent in C. elegans, and enhanced when it is over-expressed [22].
