Although much is known about long-term memory (LTM) consolidation, what puts the "long" in LTM is the exclusive feature of persisting over time. However, until recently the molecular mechanisms underneath memory persistence had never been properly studied. In rats, the protein translation inhibitor anisomycin impaired memory persistence when injected into the dorsal hippocampus 12 h after inhibitory avoidance (IA) training without affecting memory formation. Here, we also show learning-induced changes in hippocampal c-Fos, Homer 1a, Akt, CamKIIα, and ERK2 levels around 18-24 h after IA training. Thus, memory persistence is associated with a late phase of plasticity-related protein synthesis in the hippocampus.
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