A cellular model of memory reconsolidation involves reactivation-induced destabilization and restabilization at the sensorimotor synapse in Aplysia

作者:Lee Sue Hyun; Kwak Chuljung; Shim Jaehoon; Kim Jung Eun; Choi Sun Lim; Kim Hyoung F; Jang Deok Jin; Lee Jin A; Lee Kyungmin; Lee Chi Hoon; Lee Young Don; Miniaci Maria Concetta; Bailey Craig H; Kandel Eric R*; Kaang Bong Kiun
来源:Proceedings of the National Academy of Sciences of the United States of America, 2012, 109(35): 14200-14205.
DOI:10.1073/pnas.1211997109

摘要

The memory reconsolidation hypothesis suggests that a memory trace becomes labile after retrieval and needs to be reconsolidated before it can be stabilized. However, it is unclear from earlier studies whether the same synapses involved in encoding the memory trace are those that are destabilized and restabilized after the synaptic reactivation that accompanies memory retrieval, or whether new and different synapses are recruited. To address this issue, we studied a simple nonassociative form of memory, long-term sensitization of the gill-and siphon-withdrawal reflex in Aplysia, and its cellular analog, long-term facilitation at the sensory-to-motor neuron synapse. We found that after memory retrieval, behavioral long-term sensitization in Aplysia becomes labile via ubiquitin/proteasome-dependent protein degradation and is reconsolidated by means of de novo protein synthesis. In parallel, we found that on the cellular level, long-term facilitation at the sensory-to-motor neuron synapse that mediates long-term sensitization is also destabilized by protein degradation and is restabilized by protein synthesis after synaptic reactivation, a procedure that parallels memory retrieval or retraining evident on the behavioral level. These results provide direct evidence that the same synapses that store the long-term memory trace encoded by changes in the strength of synaptic connections critical for sensitization are disrupted and reconstructed after signal retrieval.

  • 出版日期2012-8-28