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Memory Reconsolidation and Extinction Have Distinct Temporal and Biochemical Signatures
The temporal dynamics of memory reconsolidation are dependent on the strength and age of the memory, such that younger and weaker memories are more easily reconsolidated than older and stronger memories.
Behavioral phenotypes of inbred mouse strains: implications and recommendations for molecular studies
Strain distributions are described for open field activity, learning and memory tasks, aggression, sexual and parental behaviors, acoustic startle and prepulse inhibition, and the behavioral actions of ethanol, nicotine, cocaine, opiates, antipsychotics, and anxiolytics.
The Involvement of the Anterior Cingulate Cortex in Remote Contextual Fear Memory
Although the molecular, cellular, and systems mechanisms required for initial memory processing have been intensively investigated, those underlying permanent memory storage remain elusive. We
Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis
The results presented here reveal a biological basis for some of the cognitive deficits associated with tuberous sclerosis, and they show that treatment with mTOR antagonists ameliorates cognitive dysfunction in a mouse model of this disorder.
Matrix Metalloproteinase-9 Is Required for Hippocampal Late-Phase Long-Term Potentiation and Memory
A novel role for MMP-9 is demonstrated in hippocampal synaptic physiology, plasticity, and memory and integrin function-blocking reagents prevent an M MP-9-mediated potentiation of synaptic signal strength.
Dnmt1 and Dnmt3a maintain DNA methylation and regulate synaptic function in adult forebrain neurons
Dnmt1 and Dnmt3a are required for synaptic plasticity, learning and memory through their overlapping roles in maintaining DNA methylation and modulating neuronal gene expression in adult CNS neurons.
CREB required for the stability of new and reactivated fear memories
It is found that CREB is crucial for the consolidation of long-term conditioned fear memories, but not for encoding, storage or retrieval of these memories.
Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1
The results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition.
Selective cognitive dysfunction in acetylcholine M1 muscarinic receptor mutant mice
Memory in mice with a null mutation of the gene coding the M1 receptor, the most densely distributed muscarinic receptor in the hippocampus and forebrain is examined, suggesting that the M 1 receptor is specifically involved in memory processes for which the cortex and hippocampus interact.