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

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 an...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2012-08, Vol.109 (35), p.14200-14205
Main Authors: 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
Format: Article
Language:English
Subjects:
Animal behavior
Animal cognition
Animals
Aplysia
Behavior, Animal - physiology
Behavioral neuroscience
Biological Sciences
Cells, Cultured
Cellular biology
Coculture Techniques
Electroshock
Excitatory Postsynaptic Potentials - physiology
Fear - physiology
Gills - innervation
Memory
Memory - drug effects
Memory - physiology
Memory recall
Models, Animal
Mollusks
Motor Neurons - cytology
Motor Neurons - physiology
Nerve Tissue Proteins - biosynthesis
Neuronal Plasticity - drug effects
Neuronal Plasticity - physiology
Neurons
Protein synthesis
Reflex - physiology
Retraining
Sensitization
Sensory neurons
Sensory Receptor Cells - cytology
Sensory Receptor Cells - physiology
Serotonin - pharmacology
Serotonin Receptor Agonists - pharmacology
Synapses
Synapses - physiology
Vehicles
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Summary: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, longterm 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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1211997109