Recently it has been shown that hippocampal protein degradation via the ubiquitin proteasome system (UPS) is a prerequisite for reconsolidation of associative fear memory. Nevertheless the results for the role of hippocampal UPS mediated protein degradation in the consolidation of memory remain contradictory. Now Jarome et al. present data, suggesting that consolidation of fear memory depends on NMDA Receptor-triggered protein degradation in the amygdala. Further they show that the time courses (molecular marker & behavioral pharmacology) of protein degradation and protein synthesis induced by acquisition of fear memory are similar, suggesting that the processes are coupled. This is supported by their findings that MOV10 (a protein which silences synaptic protein synthesis) is tagged for degradation induced by acquisition. Concerning reconsolidation they confirm existing results mentioned above and add evidence that these processes are NMDAR dependent. Interestingly they show that the same targets tagged for degradation induced by acquisition (MOV10 & Shank) are also tagged induced by retrieval. The results of this comprehensive study show that consolidation and reconsolidation of fear memory depend on protein degradation in the amygdala.
Jarome, T., Werner, C., Kwapis, J., & Helmstetter, F. (2011). Activity Dependent Protein Degradation Is Critical for the Formation and Stability of Fear Memory in the Amygdala PLoS ONE, 6 (9) DOI: 10.1371/journal.pone.0024349
Tags: Amygdala, Fear, Memory, NMDAR, proteasome
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