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 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.
Department of Biological Sciences, National Creative Research Initiative Center for Memory, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea.
Sue-Hyun
SH
Lee
Chuljung
C
Kwak
Jaehoon
J
Shim
Jung-Eun
JE
Kim
Sun-Lim
SL
Choi
Hyoung F
HF
Kim
Deok-Jin
DJ
Jang
Jin-A
JA
Lee
Kyungmin
K
Lee
Chi-Hoon
CH
Lee
Young-Don
YD
Lee
Maria Concetta
MC
Miniaci
Craig H
CH
Bailey
Eric R
ER
Kandel
Bong-Kiun
BK
Kaang
D000818:Animals; D001048:Aplysia; D001522:Behavior, Animal / Q000502:physiology; D002478:Cells, Cultured; D018920:Coculture Techniques; D004597:Electroshock; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D005239:Fear / Q000502:physiology; D005880:Gills / Q000294:innervation; D008568:Memory / Q000187:drug effects / Q000502:physiology*; D023421:Models, Animal; D009046:Motor Neurons / Q000166:cytology / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D012018:Reflex / Q000502:physiology; D011984:Sensory Receptor Cells / Q000166:cytology / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D013569:Synapses / Q000502:physiology*
D009419:Nerve Tissue Proteins; D017366:Serotonin Receptor Agonists; D012701:Serotonin