Geon Memory Extinction and Posttraumatic Stress Disorder Papers



According to the CABT Hypothesis, elevated GluN2B/GluN2A ratio in the dendritic branches that encode a memory should promote extinction of the memory. Brain-derived neurotrophic factor (BDNF) has been shown to increase localization of GluN2B-containing NMDARs to the dendritic membrane, which may explain why BDNF promotes extinction. Calcineurin has also been demonstrated to activate the transcription factor, nuclear factor of activated T-cells (NFAT), thereby enhancing extinction. BDNF is a key target of NFAT. Posttraumatic stress disorder (PTSD) is characterized by the inability to forget or extinguish traumatic events. As expected, lower BDNF level is prone to develop PTSD. Glucocorticoid, which can be enhanced by stress, is known to facilitate PTSD. In support of this hypothesis, glucocorticoid has been shown to suppress the BDNF level. On the other hand, PTSD can also arise from strengthening of traumatic memory. NF-κB plays a key role in memory strengthening. Therefore, the pathways leading to activation of NF-κB should exacerbate PTSD, as observed for the metabotropic glutamate receptor subtype 5 (mGluR5) and α1-adrenergic receptor.


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