Geon Memory Extinction and Retrieval: An Overview Papers



The extinction training has been shown to activate the signaling pathways of calcineurin and extracellular signal-regulated kinase (ERK). Both pathways lead to upregulation of brain-derived neurotrophic factor (BDNF), which is known to play a crucial role in memory extinction. Exactly how BDNF promotes memory extinction remains unclear. This paper proposes that the key factor could be the subunit composition of NMDA receptors (NMDARs). Available evidence suggests that BDNF increases the trafficking of GluN2B-containing NMDARs to the dendritic membrane, consistent with the CABT hypothesis, which posits that a high GluN2B/GluN2A ratio at the dendritic membrane is prone to develop memory extinction. This hypothesis is based on the finding that the CABT complex (consisting of a CRMP2 monomer and a tubulin heterodimer) binds only to the GluN2B-containing NMDARs, not GluN2A-NMDARs. Therefore, only the GluN2B-NMDARs can be blocked by CABT to inhibit memory retrieval. The binding between CABT and GluN2B is regulated by protein kinase A (PKA), which explains why PKA can influence memory extinction and retrieval.


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