Geon Memory Extinction, Retrieval and Consolidation:
An Overview



This paper presents an overview for the mechanisms of memory extinction, retrieval and consolidation. Memory extinction may result from the inhibition of NMDA receptors by the tubulin/CRMP2 complex, which could bind to the GluN2B subunit at Serine 1166 (S1166), a phosphorylation site of protein kinase A (PKA). Phosphorylation of S1166 by PKA may cause dissociation of tubulin/CRMP2 from GluN2B, thereby facilitating retrieval, whereas dephosphorylation of S1166 by calcineurin promotes extinction. It has been well documented that memory retrieval often leads to memory consolidation. According to the Microtubule Track hypothesis, the "very long-term memory" (> 1 month) is stored in specific microtubule tracks directing PSD-95 trafficking from the soma toward potentiated spines. Therefore, memory consolidation should involve remodeling of microtubule tracks, which can be achieved by tubulin and CRMP2 dissociated from GluN2B, as they are known to play a pivotal role in microtubule polymerization. During consolidation, PKMĪ¶ is required to maintain an elevated level of synaptic AMPARs, for otherwise the memory would not be retrieved and consolidated, even after tubulin/CRMP2 dissociates from GluN2B.


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